lactoferrin and Helicobacter-Infections

Several randomized-controlled trials (RCTs) have sought to determine the efficacy of bovine lactoferrin in Helicobacter pylori eradication with equivocal results.. To evaluate the effect of bovine lactoferrin supplementation in H. pylori eradication.. Electronic databases, reviews, bibliographies, abstracts and conference proceedings were searched. Included trials had to be randomized or quasi-randomized and controlled, using bovine lactoferrin in the intervention group, treating Helicobacter-infected subjects and evaluating eradication of H. pylori as an outcome.. The search identified five eligible RCTs (of 169). Data were available for 682 subjects (bovine lactoferrin group-n = 316; control group-n = 366). The pooled odds ratio (five studies) for eradication by intention-to-treat analysis was 2.22 (95% CI 1.44-3.44; P = 0.0003) using the fixed effects model (FEM) and 2.24 (95% CI 1.15-4.35; P = 0.0003) using the random effects model (REM) (Cochran's Q = 6.83; P = 0.145). The pooled risk difference was 0.11 (95% CI 0.05-0.16; P = 0.0001) by FEM (Cochran's Q = 6.67; P = 0.154) and 0.10 (95% CI 0.04-0.17; P = 0.0023) by REM. There was no significant difference in incidence of adverse effects.. Bovine lactoferrin potentially improves H. pylori eradication rates without any impact on adverse effects, but available evidence is limited and further research is necessary to confirm the findings.

Topics: Anti-Bacterial Agents; Dietary Supplements; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Randomized Controlled Trials as Topic

Recent evidence shown that lactoferrin could exert an antimicrobial effect against Helicobacter pylori both in vitro and in vivo models. To systematically evaluate whether adding lactoferrin to H. pylori eradication regimens could improve eradication rates and reduce side-effects during anti-H. pylori treatment.. Eligible articles were identified by searches of electronic databases. We included all randomized trials comparing lactoferrin supplementation to placebo or no treatment during anti-H. pylori regimens. Statistical analysis was performed with Review Manager 5.0.10. Subanalysis/Sensitivity analysis was also performed.. We identified nine randomized trials (n = 1343). Pooled H. pylori eradication rates were 86.57% (95% confidence interval (CI) = 83.99-89.15%) and 74.44% (95% CI = 71.14-77.74%) for patients with or without lactoferrin by intention-to-treat analysis, respectively, the odds ratio (OR) was 2.26 (95% CI = 1.70-3.00); the occurrence of total side-effects was 9.05% (95% CI = 6.83-11.27%) and 16.28% (95% CI = 13.43%-19.13%) for groups with or without lactoferrin, especially for nausea, the summary OR was 0.15 (95% CI = 0.04-0.54).. Our review suggests that supplementation with lactoferrin could be effective in increasing eradication rates of anti-H. pylori therapy, and could be considered helpful for patients with eradication failure. Furthermore, lactoferrin shows a positive impact on H. pylori therapy-related side-effects.

Topics: Anti-Bacterial Agents; Dietary Supplements; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Randomized Controlled Trials as Topic

Topics: Animals; Anti-Bacterial Agents; Disease Models, Animal; Drug Resistance, Bacterial; Drug Therapy, Combination; Enzyme Inhibitors; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Proton Pump Inhibitors; Randomized Controlled Trials as Topic

Lactoferrin possesses antibiotic, antiinflammatory, and immune-modulating properties that may be active against the gastritis-, ulcer- and cancer-inducing bacterium Helicobacter pylori. In vitro testing of bovine and human lactoferrin by several laboratories has shown significant bacteriostatic and bactericidal activity. Subsequent in vivo testing of bovine lactoferrin in animal models of H. pylori infection has shown beneficial effects of this agent. Our laboratory has utilized a mouse model that is infected with the feline strain of this bacterium, H. felis. The resulting gastritis that develops in this model and the effects of bovine lactoferrin and recombinant human lactoferrin (from Aspergillus niger var. awamori, Agennix Inc., Houston, Tex.) treatment were assessed by various measures. Infected animals treated with orally administered lactoferrin showed reversals in all parameters. In addition, when recombinant human lactoferrin was used in combination with low doses of amoxicillin or tetracycline, there was an enhancement in gastritis-reducing activity. Possible mechanisms for these effects of lactoferrin are discussed. Lactoferrin has significant, orally active in vivo actions and should be further investigated for clinical situations involving Helicobacter infections where it may have utility when administered alone and also when given in combination with established antibiotic agents.

Topics: Animals; Anti-Bacterial Agents; Cell Division; Clinical Trials as Topic; Disease Models, Animal; Gastritis; Helicobacter; Helicobacter Infections; Humans; Lactoferrin

Since the discovery of H. pylori in 1982 (MARSHALL 1983; WARREN 1983), research on the mechanisms of virulence of H. pylori has advanced substantially. It is now well established that urease and flagella are virulence factors of H. pylori. Although known for some time to be toxic to epithelial cells in vitro, VacA has only recently been established as a virulence factor. The cag pathogenicity island has also emerged as another virulence contender, although the specific genes involved in virulence are still being determined. Other possible virulence factors, not yet confirmed by gene disruptions, are hapA, katA, sodA, cagA, and iron-regulated genes. As of yet, no adhesins have been confirmed as being important for in vivo survival of H. pylori. With the sequence of the H. pylori genome in hand, it should be possible to more easily determine the role of specific genes in virulence. Genes of immediate interest are the OMPs, which may under go phase and antigenic variation and may represent adhesins. Additionally, virulence-related orthologs and vacA-related genes may provide some interesting findings. Once we define the genes that contribute to H. pylori virulence, we may be able to more easily develop novel therapeutic drugs or vaccines to treat and prevent H. pylori infection.

Topics: Adhesins, Bacterial; Antigens, Bacterial; Bacterial Proteins; Catalase; Helicobacter Infections; Helicobacter pylori; Hemagglutinins; Humans; Lactoferrin; Lectins; Lipopolysaccharides; Lipoproteins; Movement; Mutation; Siderophores; Superoxide Dismutase; Urease; Virulence

Bovine lactoferrin addition to regimens of Helicobacter pylori treatment has been tried, with conflicting results.. To assess the effect of bovine lactoferrin in addition to the anti-H. pylori treatment.. We enrolled 400 H. pylori-infected patients who were randomized into 4 equal groups: (A): proton-pump-based triple therapy (PpTT) for 2 weeks, (B): sequential therapy for 2 weeks, (C): proton-pump-based triple therapy plus bovine lactoferrin for 2 weeks, and (D): sequential therapy plus bovine lactoferrin for 2 weeks.. In the per-protocol analysis, the success in groups A, B, C, and D were 70.3%, 82.8%, 85.6%, and 94.5%, respectively (P < .001). The treatment success rate for the sequential therapy plus bovine lactoferrin regimen was significantly higher than that with sequential therapy alone (94.5% vs. 82.8%, P = .013). The same applied for proton-pump-based triple therapy (85.6% vs. 70.3%, P = .014). The addition of bovine lactoferrin and the presence of endoscopic corpus gastritis were independent predictors for successful eradication of H. pylori.. Bovine lactoferrin could hasten the effectiveness of the proton-pump-based triple therapy or sequential therapy for H. pylori eradication.

Topics: Anti-Bacterial Agents; Drug Therapy, Combination; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Treatment Outcome

Sequential therapy (ST) seems to offer higher success rates than triple therapy (TT) in the eradication of Helicobacter pylori (H. pylori) infection. However, from the standpoint of therapeutic compliance, there is no difference between the two treatments. Adjuvant treatment (especially with probiotics (PB) and lactoferrin (LF)) has often improved compliance and eradication rates in patients subjected to TT, while ST had never been used in association with adjuvants.. Over a period of 2 years, we randomized and divided 227 consecutive adult patients with H. pylori infection into three groups. The patients were given ST with the addition of adjuvants, as follows: group A (ST + placebo), group B (ST + LF + PB), and group C (ST + PB). Our goal was to assess therapeutic compliance, so we prepared a questionnaire to help determine the severity of the side effects. We also determined the eradication rates for the groups.. Patients with ST + placebo had the worst compliance as compared with the other two groups in terms of the absence of symptoms (p < .001 between B and A; p = .001 between C and A) and the presence of intolerable symptoms (p = .016 between B and A; p = .046 between C and A). The differences between the values for the treated groups and those for the placebo group were statistically significant. On the other hand, there was no statistically significant difference in compliance between groups B and C. The eradication rate was similar for the three groups.. Probiotics associated with ST provide optimum therapeutic compliance compared with the placebo and, despite the need to take a larger number of tablets, they should be taken into consideration as an adjuvant to therapy for H. pylori infection. The addition of LF to the PB did not bring about any further improvements in compliance. As compared with the placebo, the eradication rate of ST did not improve by adding LF + PB or by using PB alone.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anti-Bacterial Agents; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Patient Compliance; Probiotics; Treatment Outcome; Young Adult

To evaluate whether the addition of a probiotic could improve Helicobacter pylori (H.P.) eradication rates and reduce the side effects of treatment in children.. Between July 2008 and July 2011 all patients with a clinical, laboratory and endoscopic diagnosis of H.P. positive gastritis referred to our Unit were included in the study. Patients suffering from allergy to any of drugs used in the study, with previous attempts to eradicate H.P. and those who received antibiotics, PPIs or probiotics within 4 weeks were excluded from the present study. Patients were randomized into two therapy regimens (group A and B): both groups received standard triple treatment (omeprazole, amoxicillin and clarithromycin) while only group B patients were also given a probiotic (Probinul - Cadigroup). Patients compliance was evaluated at the end of the treatment. Successful eradication was defined as a negative 13 C-urea breath test (C13-ubt) result four weeks after therapy discontinuation.. A total of 68 histopathologically proven H.P.-infection children (32 male and 36 females) were included in the study. All of the patients in both groups used more than 90% of the therapies and no patients were lost at follow up. All side effects were selflimiting and disappeared once the therapy was terminated. Epigastric pain was observed in 6 (17.6%) group A vs 2 (5.8%) group B patients (P<0.05), nausea in 3 (8.8%) group A vs 1 (2.9%) group B patients (P<0.05); vomiting and diarrhea were observed in 2(5.8%) and 8 (23.5%) group A patients, respectively and never in group B (P<0.05). There was no significant difference between the two groups in terms of constipation (5.8% in group A and B). Four weeks after the completion of therapy, 56/68 patients (82.3%) tested negative for H.P. on C13-ubt. H.P. was eradicated in 26 patients (76.4%) in group A and in 30 patients (88.2%) in group B. There was no significantly difference in the rate of H.P. eradication between group A and group B (p=0.1), although the success rate for H.P. eradication was higher in group B than in group A.. The addition of a probiotic formula to triple therapy significantly decreased the frequency of epigastric pain, nausea, vomiting and diarrhea.

Topics: Anti-Bacterial Agents; Anti-Infective Agents; Child; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Probiotics; Treatment Outcome

Helicobacter pylori is causally associated with gastritis and peptic ulcer diseases. Recent data (meta-analysis) have demonstrated that triple therapy with amoxicillin, clarithromycin, and a proton pump inhibitor has an eradication rate of only 74-76% and new therapeutic protocols may be necessary. The aim of this study was to examine whether adding bovine lactoferrin (bLf) and probiotics (Pbs) to the standard triple therapy for H. pylori infection could improve the eradication rate and reduce side effects.. H. pylori infection was diagnosed in 206 patients: in 107 based on an upper endoscopy exam and a rapid urease test, and in 99 by means of the H. pylori stool antigen-test and the C(13) urea breath test (C(13) UBT). The patients were randomized into two groups: 101 patients (group A) underwent standard triple eradication therapy (esomeprazole, clarithromycin, amoxicillin), while 105 patients (group B) underwent a modified eradication therapy (standard triple eradication therapy plus bLf and Pb). Successful eradication therapy was defined as a negative C(13) UBT 8 wk after completion of the treatment. Results were evaluated by intention-to-treat (ITT) and per-protocol (PP) analysis. Data were evaluated and considered positive when P<0.05.. At the end of the study 175/206 patients showed negative C(13) UBT results. According to intention-to-treat analysis, the infection was eradicated in 73/101 patients from Group A and in 93/105 from Group B. PP analysis showed 73/96 patients from Group A and 93/101 from Group B to have been successfully treated. More patients from group A than from group B reported side effects from their treatment (P<0.05).. The results of our study suggest that the addition of bLf and Pbs could improve the standard eradication therapy for H. pylori infection--bLf serving to increase the eradication rate and Pbs to reduce the side effects of antibiotic therapy.

Topics: Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Breath Tests; Clarithromycin; Drug Therapy, Combination; Endoscopy, Gastrointestinal; Esomeprazole; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Probiotics; Prospective Studies; Treatment Outcome

Up to 35% of H. pylori-positive patients remain infected after a first eradication attempt. Lactoferrin, a natural anti-bacterial glycoprotein, seems a promising tool in treating H. pylori infection, but it has never been used in second-line treatment.. A prospective, randomized study was conducted on 70 consecutive patients with persistent H. pylori infection after failure of the first standard treatment schedule. All patients were randomly treated with ranitidine bismuth citrate (RBC, 400 mg b.d.), esomeprazole (40 mg/day), amoxycillin (1 g t.d), and tinidazole (500 mg b.d.) without (group A) or with (group B) supplementation of bovine lactoferrin (200 mg b.d). One month after conclusion of therapy, endoscopy was performed in those patients for whom the examination was clinically relevant. The remaining patients were checked by 13C-urea breath test.. Sixty-seven patients were fully compliant and completed the study (33, i.e. 94.28%, in group A and 34, 97.14%, in group B). One group A patient (2.85%) was excluded for protocol violation and one group B patient (2.85%) was lost to follow-up. H. pylori eradication was obtained in 31/33 (on intention-to-treat: 88.57%, 95%CI: 87-99%) group A patients and in 33/34 (on intention-to-treat: 94.28%, 95%CI: 86-100%) group B patients (p=ns). 16/68 patients (23.53%) experienced side effects (29.41% in group A and 17.64% in group B, p= 0.05).. Lactoferrin supplementation was found effective in reducing side-effect incidence. Moreover, it seems capable of achieving a slight (and not statistically significant) improvement in eradicating H. pylori when used in second-line treatment.

Topics: Adult; Aged; Amoxicillin; Anti-Bacterial Agents; Bismuth; Breath Tests; Endoscopy, Gastrointestinal; Esomeprazole; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Prospective Studies; Ranitidine; Tinidazole

Curcumin is the principal element of turmeric powder extracted from the root of Curcuma longa. Studies on curcumin have demonstrated some anti-Helicobacter pylori activity as well as immunomodulating properties. N-acetylcysteine and lactoferrin with their respective mucolytic and antibacterial activities might also be effective in H. pylori eradication therapy.. To determine if a 7-day non-antibiotic therapy comprised of curcumin, lactoferrin, N-acetylcysteine, and pantoprazole was effective for eradication of H. pylori infection and reduction of gastric inflammation, assessed by serum pepsinogens and relief of symptoms.. Twenty-five consecutive H. pylori-positive patients (12 males, mean age 50 +/- 12 years, range 31-76) with functional dyspepsia were enrolled. Patients were administered for 7 days curcumin 30 mg b.i.d., bovine lactoferrin 100 mg b.i.d., N-acetylcysteine 600 mg b.i.d., and pantoprazole 20 mg b.i.d. H. pylori status and upper gastrointestinal symptoms were assessed by (13)C-urea breath test and a scale of upper gastrointestinal symptoms intensity (absent, mild, moderate, and severe), as well as a blood test for serum pepsinogens (sPGI, sPGII), gastrin-17 (G-17), and anti-H. pylori IgG (IgG-Hp) at baseline (T0) and after 2 months (T1).. Three of 25 patients (12%) were cured of H. pylori infection. A significant decrease in the overall severity of symptoms (T0: 6, interquartile range [IQR]: 4.5-8; T1: 2, IQR: 2-3; p < or = .001), and sPGII (T0: 16 microg/L, IQR: 13-22; T1: 10 microg/L, IQR: 8-16; p < or = .001) and sPGI (T0: 82 microg/L, IQR: 67-97; T1: 74 microg/L, IQR: 62-94; p = .02) levels were observed after 2 months of the treatment. IgG and G-17 values did not significantly decrease after 2 months.. This novel therapy was not effective for H. pylori eradication. However, despite the bacterium persistence, significant improvement of dyspeptic symptoms and reduction of serologic signs of gastric inflammation were observed after 2 months at the end of the 7-day treatment schedule.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Acetylcysteine; Adult; Aged; Curcumin; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Pantoprazole; Treatment Failure

Helicobacter pylori eradication rate following standard triple therapy is decreasing worldwide. A quadruple therapy with lactoferrin and a levofloxacin-based triple therapy has been found to achieve a very high (>90%) cure rate. This study aimed to confirm these encouraging results.. This was a prospective, open-label, randomised, multicentre, Italian study enrolling consecutive H. pylori infected patients. The infection at entry was assessed by endoscopy and biopsies (histology plus rapid urease test) in all patients, whilst bacterial eradication was assessed by 13C-urea breath test 4-6 weeks after therapy ended. Patients were randomised to receive either a 7-day, triple therapy with rabeprazole 20mg o.d., levofloxacin 500 mg o.d., and amoxycillin 1g b.i.d. (4 tablets/day) or a 7-day quadruple therapy comprising of rabeprazole 20mg, clarithromycin 500 mg, tinidazole 500 mg plus bovine lactoferrin 200mg, all given twice daily (10 tablets/day).. Overall, 144 consecutive patients were enrolled in the study. Following the triple therapy, H. pylori infection was cured in 49 out of 72 (68.1%; 95% CI=57-79) patients and in 49 out of 71 (69.1%; 95% CI=58-80) at intention-to-treat and per protocol analyses, respectively. Following the quadruple regimen, the infection was cured in 52 out of 72 (72.2%; 95% CI=62-83) and in 52 out of 68 (76.5; 95% CI=66-87) patients at intention-to-treat and per protocol analyses, respectively. No statistically significant difference emerged between the two therapy regimens.. H. pylori eradication rate following both quadruple therapy with lactoferrin and a low-dose PPI, triple therapy with levofloxacin is disappointingly low.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Amoxicillin; Anti-Bacterial Agents; Clarithromycin; Drug Therapy, Combination; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Levofloxacin; Male; Middle Aged; Ofloxacin; Rabeprazole; Tinidazole; Treatment Outcome

Cure rates for eradication of Helicobacter pylori appear to be decreasing, thus more effective therapies must be identified.. To evaluate the efficacy of bovine lactoferrin in the treatment of H. pylori infection.. In a multicentered prospective study, 402 (mean age 52.4, range 19-84 years) H. pylori-positive patients were assigned to one of three regimens: group A - esomeprazole 20 mg b.d., clarithromycin 500 mg b.d. and tinidazole 500 mg b.d. for 7 days; group B - lactoferrin 200 mg b.d. for 7 days followed by the same schedule of group A; group C - esomeprazole 20 mg b.d., clarithromycin 500 mg b.d. and tinidazole 500 mg b.d. plus lactoferrin 200 mg b.d. for 7 days.. Of the 402 patients, 389 completed the study. Six patients were discontinued due to side effects, one patient in group B died and six patients were lost to follow up. The eradication rate (intention-to-treat analysis) was 77% in group A (105/136), 73% in group B (97/132) and 90% in group C (120/134) (chi(2)-test P < 0.01). The incidence of side effects was 9.5% in group A, 9% in group B and 8.2% in group C (chi(2)-test P = 0.1).. This study demonstrates that bovine lactoferrin is an effective adjuvant to 7-day triple therapy for eradication of H. pylori infection.

Topics: Adult; Aged; Aged, 80 and over; Animals; Anti-Bacterial Agents; Cattle; Chi-Square Distribution; Clarithromycin; Drug Administration Schedule; Drug Therapy, Combination; Esomeprazole; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Prospective Studies; Tinidazole; Treatment Outcome

Helicobacter pylori eradication rate with standard triple therapies is decreasing. Recently, lactoferrin administration has been shown to significantly increase the cure rate of 7-day rabeprazole, clarithromycin and tinidazole triple therapy. We assessed whether lactoferrin also increases the eradication rate of 7-day esomeprazole, clarithromycin and amoxycillin triple therapy as first-line treatment.. Overall, 133 consecutive patients with non-ulcer dyspepsia and H. pylori infection were randomised to receive either a standard 7-day triple therapy with esomeprazole 20mg b.i.d., clarithromycin 500 mg b.i.d. and amoxycillin 1g b.i.d. (68 patients) or a quadruple therapy comprising of the same regimen plus lactoferrin 200mg b.i.d. (65 patients). H. pylori at entry was assessed by endoscopy, while bacterial eradication was checked by (13)C urea breath test 4-6 weeks after treatment.. H. pylori eradication following standard triple therapy was achieved in 53/68 (77.9%; 95% CI = 68-88) and in 53/66 (80.3%; 95% CI = 71-89) patients at ITT and PP analyses, respectively. Following the quadruple regimen, the infection was cured in 50/65 (76.9%; 95% CI = 67-87) and 50/64 (78.1%; 95% CI = 68-88) patients at ITT and PP analyses, respectively. No statistically significant difference emerged between the two therapeutic regimens, both at ITT (p = 0.9) and PP analyses (p = 0.9). Side effects were complained by seven (10.3%) patients and six (9.2%) patients following the triple and quadruple regimens, respectively (p = 0.9), with only one patient in the quadruple group interrupting the treatment due to side effects.. Quadruple therapy with lactoferrin did not significantly increase the H. pylori cure rate of standard 7-day clarithromycin-amoxycillin based triple therapy in non-ulcer dyspepsia patients.

Topics: Amoxicillin; Anti-Bacterial Agents; Clarithromycin; Drug Therapy, Combination; Dyspepsia; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Prospective Studies

Bovine lactoferrin (bLF) has antibacterial activity against Helicobacter pylori in vitro and is effective to suppress bacterial colonization in mice. The aim of our study was to evaluate the efficacy of orally administered bLF on H. pylori colonization in humans by a randomized, double-blind, placebo-controlled study. Fifty-nine healthy subjects positive for H. pylori infection were recruited. Subjects were randomized into two groups. The bLF group received bLF tablets at a dosage of 200 mg b.i.d. for a period of 12 weeks, and the control group received placebo tablets without bLF. The (13)C-urea breath test (UBT) was performed before, during, and at the end of administration, and again 4 weeks after administration. Positive response was defined as more than 50% decrease of the UBT value at the end of administration. Positive response was observed in 10 of 31 bLF-treated subjects (32.3%) and 1 of 28 control subjects (3.6%), indicating that the rate of positive response in the bLF group was significantly higher than that in the control group (bLF vs. control, P < 0.01). These results suggested that bLF administration is effective to suppress H. pylori colonization.

Topics: Adolescent; Adult; Animals; Breath Tests; Cattle; Child; Child, Preschool; Double-Blind Method; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Stomach; Treatment Outcome; Urea

One-week triple therapy is the most frequently recommended treatment for Helicobacter pylori infection. Eradication rate is satisfactory, nevertheless is advisable to look for more effective therapies.. To test the efficacy of a standard triple therapy plus bovine lactoferrin in the eradication of H. pylori infection.. One hundred and fifty consecutive H. pylori positive patients, suffering from dyspeptic symptoms were recruited in a 7-day triple therapy open randomised single centre study with rabeprazole, clarithromycin, tinidazole, bovine lactoferrin (group A) or rabeprazole, clarithromycin, tinidazole (group B), or a 10-day therapy with rabeprazole, clarithromycin, tinidazole (group C). H. pylori status was assessed 8 weeks after the end of the treatment by means of a 13C-urea breath test or a H. pylori stool antigen-test.. Eradication rates (intention to treat/per protocol) were: group A (92.2/95.9%), group B (71.2/72.5%) and group C (70.2/75%). The efficacy of triple therapy added with lactoferrin was significantly higher than other two regimens (p=0.01, intention to treat analysis; p=0.005, per protocol analysis).. These results suggest that lactoferrin tested in the present study was effective in curing H. pylori and could be a new agent to assist the antimicrobials in the eradication of the bacterium.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Animals; Anti-Bacterial Agents; Anti-Ulcer Agents; Antitrichomonal Agents; Benzimidazoles; Breath Tests; Cattle; Clarithromycin; Drug Administration Schedule; Drug Therapy, Combination; Feces; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Omeprazole; Proton-Translocating ATPases; Rabeprazole; Time Factors; Tinidazole

Chronic infection with Helicobacter pylori increases risk of gastric diseases including gastric cancer. Despite development of a robust immune response, H. pylori persists in the gastric niche. Progression of gastric inflammation to serious disease outcomes is associated with infection with H. pylori strains which encode the cag Type IV Secretion System (cag T4SS). The cag T4SS is responsible for translocating the oncogenic protein CagA into host cells and inducing pro-inflammatory and carcinogenic signaling cascades. Our previous work demonstrated that nutrient iron modulates the activity of the T4SS and biogenesis of T4SS pili. In response to H. pylori infection, the host produces a variety of antimicrobial molecules, including the iron-binding glycoprotein, lactoferrin. Our work shows that apo-lactoferrin exerts antimicrobial activity against H. pylori under iron-limited conditions, while holo-lactoferrin enhances bacterial growth. Culturing H. pylori in the presence of holo-lactoferrin prior to co-culture with gastric epithelial cells, results in repression of the cag T4SS activity. Concomitantly, a decrease in biogenesis of cag T4SS pili at the host-pathogen interface was observed under these culture conditions by high-resolution electron microscopy analyses. Taken together, these results indicate that acquisition of alternate sources of nutrient iron plays a role in regulating the pro-inflammatory activity of a bacterial secretion system and present novel therapeutic targets for the treatment of H. pylori-related disease.

Topics: Animals; Disease Models, Animal; Epithelial Cells; Gastric Mucosa; Gerbillinae; Helicobacter Infections; Helicobacter pylori; Immunity, Innate; Interleukin-8; Iron; Lactoferrin; Protein Isoforms; Type IV Secretion Systems

To evaluate the in vitro antimicrobial/antivirulence action of bovine lactoferrin and its ability to synergize with levofloxacin against resistant Helicobacter pylori strains and to analyse the effect of levofloxacin, amoxicillin and esomeprazole with and without bovine lactoferrin as the first-line treatment for H. pylori infection.. The bovine lactoferrin antimicrobial/antivirulence effect was analysed in vitro by MIC/MBC determination and twitching motility against six clinical H. pylori strains and a reference strain. The synergism was evaluated using the chequerboard assay. The prospective therapeutic trial was carried out on two separate patient groups, one treated with esomeprazole/amoxicillin/levofloxacin and the other with esomeprazole/amoxicillin/levofloxacin/bovine lactoferrin. Treatment outcome was determined with the [13C]urea breath test.. In vitro, bovine lactoferrin inhibited the growth of 50% of strains at 10 mg/mL and expressed 50% bactericidal effect at 40 mg/mL. The combination of levofloxacin and bovine lactoferrin displayed a synergistic effect for all strains, with the best MIC reduction of 16- and 32-fold for levofloxacin and bovine lactoferrin, respectively. Bovine lactoferrin at one-fourth MIC reduced microbial motility significantly for all strains studied. In the in vivo study, 6 of 24 patients recruited had treatment failure recorded with esomeprazole/amoxicillin/levofloxacin (75% success, 95% CI 57.68%-92.32%), and in the group with esomeprazole/amoxicillin/levofloxacin/bovine lactoferrin, 2 out of 53 patients recruited had failure recorded (96.07% success, 95% CI 90.62%-101.38%).. Bovine lactoferrin can be considered a novel potentiator for restoring susceptibility in resistant H. pylori strains. Bovine lactoferrin added to a triple therapy in first-line treatment potentiates the therapeutic effect.

Topics: Adult; Aged; Animals; Anti-Bacterial Agents; Cattle; Drug Therapy, Combination; Female; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Levofloxacin; Male; Microbial Sensitivity Tests; Middle Aged; Proton Pump Inhibitors; Young Adult

Helicobacter pylori (H. pylori) is a highly successful bacterial pathogen, which colonizes the stomach of more than half of the world's population. To colonize and survive in such an acidic and inhospitable niche, H. pylori cells have evolved complex mechanisms to acquire nutrients from human hosts, including iron, an essential nutrient for both the pathogens and host cells. However, human cells also utilize diverse strategies in withholding of irons to prevent the bacterial outgrowth. The competition for iron is the central battlefield between pathogen and host. This mini-review summarizes the updated scenarios of the battle for iron between H. pylori and human host from a structural biology perspective.

Topics: Amino Acids; Binding Sites; Binding, Competitive; Helicobacter Infections; Helicobacter pylori; Homeostasis; Host-Pathogen Interactions; Humans; Iron; Iron-Binding Proteins; Lactoferrin; Models, Molecular; Protein Binding; Protein Conformation

The resistance of Helicobacter pylori to the antibiotic therapy poses the problem to discover new therapeutic approaches. Recently it has been stated that antibacterial, immunomodulatory, and antioxidant properties of lactoferrin are increased when this protein is surface-linked to biomimetic hydroxyapatite nanocrystals.. Based on these knowledge, the aim of the study was to investigate the efficacy of lactoferrin delivered by biomimetic hydroxyapatite nanoparticles with cell free supernatant from probiotic Lactobacillus paracasei as an alternative therapy against Helicobacter pylori infection.. Antibacterial and antinflammatory properties, humoral antibody induction, histopathological analysis and absence of side effects were evaluated in both in vitro and in vivo studies.. The tests carried out have been demonstrated better performance of lactoferrin delivered by biomimetic hydroxyapatite nanoparticles combined with cell free supernatant from probiotic Lactobacillus paracasei compared to both lactoferrin and probiotic alone or pooled.. These findings indicate the effectiveness and safety of our proposed therapy as alternative treatment for Helicobacter pylori infection.

Topics: Adsorption; Animals; Anti-Infective Agents; Biomimetic Materials; Culture Media, Conditioned; Cytokines; Drug Delivery Systems; Durapatite; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Lacticaseibacillus paracasei; Lactoferrin; Mice, Inbred BALB C; Microscopy, Electron, Transmission; Nanoparticles; Probiotics; Stomach; Treatment Outcome; X-Ray Diffraction

Helicobacter pylori (H. pylori) is a life-threatening pathogen which causes chronic gastritis, gastric ulcers and even stomach cancer. Treatment normally involves bacterial eradication; however, this type of treatment only has a rate of effectiveness of <80%. Thus, it is a matter of some urgency to develop new therapeutic strategies. Lactoferrin, a member of the transferrin family of iron-binding proteins, has been proven to be effective in removing a vast range of pathogens, including H. pylori. In the present study, we examined the effectiveness of recombinant human lactoferrin (rhLf) isolated from transgenic goats as a treatment for H. pylori in vitro and in vivo. For the in vivo experiments, BALB/c mice received an intragastric administration of 0.1 ml of a suspension of H. pylori. The mice were then divided into 4 groups: group A, treated with saline; group B, treated with 1.5 g of rhLF; group C, treated with the standard triple therapy regimen; and group D, treated with the standard triple therapy regimen plus.5 g of rhLF. Following sacrifice, the stomach tissues of the mice were histologically examined for the presence of bacteria. For the in vitro experiments, the bacteria were cultured in BHI broth and RT-qPCR and western blot analysis were carried out to determine the mRNA and protein levels of virulence factors (CagA and VacA) in the cultures. Our results revealed that rhLf not only inhibited the growth of H. pylori, but also suppressed the expression of two major virulence factors. Moreover, rhLf markedly increased bacterial eradication and effectively reduced the inflammatory response when combined with the standard triple therapy regimen. These results provide evidence supporting the use of rhLF as an adjuvant to traditional therapeutic strategies in the treatment of H. pylori.

Topics: Animals; Anti-Bacterial Agents; Drug Synergism; Gene Expression Regulation, Bacterial; Goats; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Lactoferrin; Mice; Mice, Inbred BALB C; Recombinant Proteins; Stomach

To determine gastric tissue lactoferrin (Lf) levels of Helicobacter pylori- (Hp-) positive and -negative patients and its effect on anemia.. Cases in which initial presentation was of abdominal pain and that were Hp-positive at endoscopy were included. Hp-positive cases and -negative controls were divided into two groups.. The study included 64 cases (average: 10.2 ± 0.4 years, 39 male and 25 female). Lf levels were subsequently studied on 61 cases. 45 (73.8%) of these were Hp-positive, while 16 (22.2%) were Hp-negative. In Hp-positive cases, mean staining percentages and density of glands in the antral mucosa were 45.5 ± 4.7% and 1.9 ± 0.1, respectively. Hp-negative cases showed significantly different values of 17.8 ± 4.5% and 1.3 ± 0.2, respectively. Hemoglobin and serum ferritin values of Hp-positive cases were 12.7 ± 0.2 g/dL and 32.5 ± 2 ng/mL, but these were comparable with Hp-negative cases (12.6 ± 0.1 g/dL and 30.7 ± 4.4 ng/mL).. Tissue Lf was significantly higher in Hp-positive cases compared to Hp-negative cases, but no difference was observed between the two groups with regards to hemoglobin and ferritin level. As a result, it is difficult to say that this rise in Lf plays a role in the development of iron deficiency anemia in Hp-positive patients.

Topics: Adolescent; Anemia, Iron-Deficiency; Child; Child, Preschool; Endoscopy; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Lactoferrin; Male; Pyloric Antrum

To evaluate the efficacy of bovine lactoferrin (BLf), recombinant human lactoferrin (rHLf) and desferrioxamine against Helicobacter pylori in vitro and in mice and also to determine whether BLf or rHLf alter gastric inflammation.. In vitro: Broth dilution susceptibility tests were performed using different concentrations of desferrioxamine, BLf and rHLf. Murine trials: In the prevention trial, C57BL/6 female mice were treated with BLf or rHLF, and then infected with the SS1 strain of H. pylori. In the treatment trial, mice were gavaged with either BLf, rHLf or desferrioxamine. In addition, gastric myeloperoxidase activity (MPO) was measured to assess gastric inflammation. Desferoxamine was found to have a direct bactericidal effect, while BLf and rHLf only partially suppressed H. pylori growth in vitro. However, in both prevention and treatment trials all three forms of treatment failed to reduce H. pylori load in mice. Gastric MPO activity and H. pylori load were noted to be higher with lactoferrin treatments.. Our study does not support the use of BLf or rHLF in the treatment of human H. pylori infection. Interestingly, H. pylori growth and gastric inflammation appear to be enhanced by lactoferrin treatment.. The mouse model is ideal for testing novel H. pylori eradicating agents.

Topics: Animals; Anti-Bacterial Agents; Deferoxamine; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Lactoferrin; Mice; Treatment Outcome

Topics: Amoxicillin; Anti-Bacterial Agents; Anti-Ulcer Agents; Breath Tests; Clarithromycin; Drug Therapy, Combination; Endoscopy, Gastrointestinal; Female; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Male; Middle Aged; Omeprazole; Probiotics; Treatment Outcome

Lactoferrin, a multifunctional glycoprotein, is known to have anti-microbial actions. Bovine lactoferrin and recombinant human lactoferrin have been shown to inhibit Helicobacter pylori, and more recently recombinant human lactoferrin was found to significantly increase the eradication rate of H. pylori when added to standard triple therapy.. To determine the efficacy, safety and tolerability of recombinant human lactoferrin as a therapy in suppressing or eliminating H. pylori infection in subjects with minimal upper gastrointestinal symptoms who have not previously been treated.. Nine healthy subjects with minimal upper gastrointestinal symptoms and a positive urea breath test were recruited. None of the volunteers had previously been treated for H. pylori. Subjects received 5 x 1.0 g human recombinant lactoferrin daily for 5 or 14 days. Breath tests were repeated during therapy and shortly after to check for eradication. The safety and tolerability of the drug were assessed by physical examination, by monitoring adverse events, and clinical laboratory evaluation.. No conversion of the urea breath test from positive to negative was observed and there was no consistent change in urea breath test count to indicate a possible suppression of H. pylori.. Lactoferrin, given as a single agent, does not eradicate H. pylori infection.

Topics: Adult; Breath Tests; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Middle Aged; Recombinant Proteins; Treatment Outcome; Urea

It is known that lactoferrin serves as a source of iron for Helicobacter pylori in gastric mucosa. The present study was undertaken to investigate the relationship between lactoferrin and H. pylori infection coexistent with iron-deficiency anemia by determining the lactoferrin levels in gastric biopsy specimens, and by locating the major sites of lactoferrin expression, according to the presence or absence of iron-deficiency anemia.. One hundred and one adolescents who underwent gastroduodenoscopy were divided into four groups: controls without H. pylori infection (NL; n =43); patients with H. pylori infection (HP; n = 26); patients with iron-deficiency anemia (IDA; n = 6); and patients with H. pylori gastritis and coexisting iron-deficiency anemia (HPIDA; n = 26). The gastric mucosal levels of lactoferrin were measured by immunoassay. Immunohistochemical technique was used to allow identification of the location and quantification of the lactoferrin expression.. The mucosal level of lactoferrin was highest (3.93 +/- 2.73 ng/microg protein) in HPIDA, followed by 2.67 +/- 1.79 ng/microg protein in HP, 0.59 +/- 0.57 ng/microg protein in NL and 0.14 +/- 0.10 ng/microg protein in IDA. Their multiple comparisons were statistically significant at the 0.05 level. After the eradication of H. pylori in 12 HPIDA patients who underwent follow-up endoscopy, the mean mucosal level of lactoferrin decreased significantly, while the blood hemoglobin level correspondingly increased. The major sites of lactoferrin expression by immunohistochemistry were in glands and neutrophils within epithelium. Lactoferrin was stained weakly in NL and IDA, and strongly in HP and HPIDA.. The lactoferrin sequestration in the gastric mucosa of HPIDA was remarkable, and this finding seems to give a clue that leads to the clarification of the mechanism by which H. pylori infection contributes to iron-deficiency anemia.

Topics: Adolescent; Anemia, Iron-Deficiency; Biopsy; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Lactoferrin; Male; Statistics, Nonparametric

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Animals; Benzimidazoles; Cattle; Clarithromycin; Drug Therapy, Combination; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin; Omeprazole; Rabeprazole; Tinidazole

The attachment of Helicobacter pylori to the human gastric mucosa is a complex process involving several specific structures recognised by the cell surface receptors. Sialylated multivalent high mol. wt glycoproteins have been shown to inhibit H. pylori sialic acid-specific haemagglutination. This study explored whether sialylated glycoconjugates from bovine milk could inhibit an experimental H. pylori infection in a mouse model. BALB/cA mice (6-8 weeks old) were inoculated with a mouse-passaged H. pylori strain 317p. Four weeks after infection the mice were given lactoferrin (iron-free LF or 20% iron-saturated LF) or bovine milk fat globule membrane fractions (MFGM or defatted MFGM) orally (400 mg/kg body weight) once daily for 10 days and then killed to examine for bacterial colonisation and gastritis. Mice treated with iron-free LF, 20% iron-saturated LF, MFGM or defatted MFGM showed 30%, 10%, 20% or 20% healing rates, respectively, when compared with the H. pylori-infected control. Gastric colonisation by H. pylori was remarkably decreased in all mice treated with bovine milk glycoconjugates and the inflammation score was also significantly lower in treated mice than in infected control animals. The fact that there was no significant difference between iron-free LF and iron-saturated LF or MFGM and defatted MFGM suggested that iron is not crucial for inhibition of H. pylori by lactoferrin and that the lipid part of MFGM is not important for anti-H. pylori activity. In conclusion, bovine milk glycoconjugates showed potencies to inhibit H. pylori infection in this mouse model and, therefore, could be considered as candidates for non-antibiotic strategies against H. pylori infection in man.

Topics: Animals; Cattle; Disease Models, Animal; Gastritis; Glycoconjugates; Helicobacter Infections; Helicobacter pylori; Lactoferrin; Mice; Mice, Inbred BALB C; Milk; Stomach

Recombinant human lactoferrin possesses in-vitro antibiotic and anti-inflammatory activity similar to the native form. It was tested for in-vivo activity in mice infected with the gastritis-inducing bacterium Helicobacter felis. A two-week course of treatment with lactoferrin was sufficient to partially reverse both infection-induced gastritis and the infection rate, and fully reverse gastric surface hydrophobicity changes. A comparison of lactoferrin with amoxicillin and standard triple therapy revealed no differences in infection rate. These results show that recombinant human lactoferrin is effective in a mouse model of Helicobacter infection, and support further testing of this promising agent for this application.

Topics: Amoxicillin; Animals; Body Weight; Dose-Response Relationship, Drug; Gastritis; Helicobacter; Helicobacter Infections; Humans; Lactoferrin; Mice; Mice, Inbred C57BL; Organ Size; Penicillins; Recombinant Proteins; Stomach; Time Factors

Increasing antibiotic resistance has begun to impair our ability to cure Helicobacter pylori infection.. To evaluate orally administered novel therapies for the treatment of H. pylori infection.. Healthy H. pylori infected volunteers received: (a) hyperimmune bovine colostral immune globulins, (b) an oligosaccharide containing an H. pylori adhesion target, Neu5Aca2-3Galb1-4Glc-(3'-sialyllactose), or (c) recombinant human lactoferrin. Outcome was assessed by urea breath test or histological assessment of the number of H. pylori present.. None of the novel therapies appeared effective and no adverse events occurred.. Although in vitro data appeared promising, in vivo results were disappointing. Higher doses, longer duration of therapy, adjunctive acid suppression, or a combination could possibly yield better results.

Topics: Adjuvants, Immunologic; Administration, Oral; Adult; Aged; Animals; Anti-Ulcer Agents; Breath Tests; Cattle; Colostrum; Female; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Lactoferrin; Lactose; Male; Middle Aged; Recombinant Proteins; Sialic Acids; Treatment Outcome; Urea

It remains unclarified whether bovine lactoferrin (bLF) can exert a therapeutic effect on the host infected with Helicobacter pylori.. Germfree BALB/c mice were orally inoculated with H. pylori to induce infection. Three weeks after infection the mice were given bLF orally once daily for 2 or 4 weeks and were then killed to examine the bacterial number in the stomach and the serum antibody titer to H. pylori. To count the number of epithelium-bound H. pylori, the resected stomach was agitated in phosphate-buffered saline to remove non-bound H. pylori before bacterial enumeration.. The administration of 10 mg bLF for 3 to 4 weeks decreased the number of H. pylori in the stomach to one-tenth and also exerted a significant inhibitory effect on the attachment of H. pylori to the stomach. As a result, the serum antibody titer to H. pylori, whose level is presumed to represent the size of the immune response by the host, thereby reflecting the degree of bacterial attack, decreased to an undetectable level.. These findings suggest that bLF exerts an inhibitory effect on colonizing H. pylori by detaching the bacterium from the gastric epithelium and by exerting a direct anti-bacterial effect.

Topics: Animals; Cattle; Enzyme-Linked Immunosorbent Assay; Gastritis; Germ-Free Life; Helicobacter Infections; Helicobacter pylori; Lactoferrin; Male; Mice; Mice, Inbred BALB C

To investigate a potential new treatment for gastric Helicobacter pylori infection, we have examined the use of the natural antibiotic lactoferrin, found in bovine milk, for activity against Helicobacter species both in vitro and in vivo. Lactoferrin was bacteriostatic to H. pylori when cultured at concentrations > or =0.5 mg/ml. Growth of H. pylori was not inhibited by another milk constituent, lysozyme, or by a metabolite of lactoferrin, lactoferricin B, but growth was inhibited by the iron chelator deferoxamine mesylate. Lactoferrin inhibition of growth could be reversed by addition of excess iron to the medium. Lactoferrin in retail dairy milk was found to be more stable intragastrically than unbuffered, purified lactoferrin. Treatment of H. felis-infected mice with lactoferrin partially reversed mucosal disease manifestations. It is concluded that bovine lactoferrin has significant antimicrobial activity against Helicobacter species in vitro and in vivo. Bovine lactoferrin should be further investigated for possible use in H. pylori infections in man.

Topics: Animals; Anti-Bacterial Agents; Cattle; Deferoxamine; Dose-Response Relationship, Drug; Enzyme-Linked Immunosorbent Assay; Female; Helicobacter Infections; Helicobacter pylori; Hydrogen-Ion Concentration; Lactoferrin; Male; Mice; Mice, Inbred C57BL; Rats; Rats, Sprague-Dawley

Lactoferrin (Lf) is an iron-binding glycoprotein present in milk, lacrimae, saliva, and gastroduodenal secretions. In vitro studies disclosed contradicting results regarding the relation of Lf with Helicobacter pylori (HP) infection. This study aimed to investigate the relationship between the gastric mucosal concentration of Lf and HP infection of the stomach. The relationship of the gastric mucosal level of Lf with the gastric mucosal concentration of interleukin-8 (IL-8) and with the intragastric ammonia levels was also assessed. In addition, the gastric mucosal Lf levels before and after irradication of HP infection were also evaluated.. This study was composed of 27 HP-positive and 12 HP-negative patients with chronic gastritis. Gastric mucosal biopsy specimens were obtained from all subjects by endoscopy, and the degree of histological inflammatory changes were assessed according to the Sydney system. The gastric mucosal levels of Lf and IL-8 were measured by immunoassays. Assessment of the effect of therapy on the gastric mucosal level of Lf was performed in 10 patients with HP-associated duodenal ulcer.. Lf, IL-8, and ammonia levels were significantly higher in patients with HP-positive gastritis compared with those with HP-negative gastritis in both the antrum and the gastric body. Histologically, the degree of inflammatory changes correlated significantly with the Lf levels in the gastric mucosa. Furthermore, the degree of HP colonization was more significant in biopsy samples from the antrum than in those from the corpus of the stomach. The gastric mucosal levels of Lf and IL-8 correlated significantly in the antrum and the gastric body. The ammonia intragastric level significantly correlated with the mucosal Lf level in the antrum and in the gastric body. Therapy significantly decreased the Lf levels in the gastric mucosa of the antrum (p < 0.005) and the gastric body (p < 0.005).. The results of the present investigation showed, for the first time in vivo, that Lf concentration is increased in the biopsy specimens of patients with HP-related gastritis, and that the levels of Lf correlate significantly with the degree of inflammation of the gastric mucosa. The gastric mucosal level of Lf may constitute an excellent marker of HP infection.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Ammonia; Anti-Bacterial Agents; Anti-Ulcer Agents; Biomarkers; Biopsy; Chronic Disease; Clarithromycin; Duodenal Ulcer; Female; Follow-Up Studies; Gastric Juice; Gastric Mucosa; Gastritis; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Lactoferrin; Lansoprazole; Male; Metronidazole; Middle Aged; Omeprazole; Pyloric Antrum

Recently, in vitro studies suggested that lactoferrin (Lf) might play an important role in the physiopathology of Helicobacter pylori-associated gastritis. However, whether Lf is present in the gastric juice and its relationship with H. pylori infection have not as yet been reported. In the present investigation the presence of Lf in gastric juice and its correlation with H. pylori infection were assessed.. This study comprised 30 H. pylori-positive and 14-negative patients with chronic gastritis. Gastric juice levels of Lf were measured with enzyme-linked immunoassays. Gastric juice concentration of Lf was also investigated in accordance with the histologic findings of biopsy specimens in the gastric body and antrum.. Lf concentration in gastric juice was significantly higher in H. pylori-positive than in -negative patients (P = 0.033). The pH values are known to influence the levels of Lf. However, intragastric Lf levels were also significantly increased in H. pylori-positive patients as compared with H. pylori-negative patients after correcting the Lf levels for pH values (P = 0.029) or after adjusting the pH values of the gastric juice with NaHCO3 solution in both groups of patients (P = 0.0007). In addition, the gastric juice levels of Lf correlated significantly with the gastric mucosal concentrations of Lf in the gastric body (P < 0.005, r = 0.568) and the antrum (P < 0.05, r = 0.401).. This study showed for the first time that Lf is present in gastric juice and that it correlates with H. pylori infection. Lf may constitute a good marker for H. pylori-associated gastritis. Although correlation does not prove causation, this study suggests that Lf might play an important role in the physiopathology of H. pylori-associated gastritis.

Topics: Biomarkers; Biopsy; Case-Control Studies; Enzyme-Linked Immunosorbent Assay; Gastric Juice; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Lactoferrin

Topics: Antibody Formation; Biopsy; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulins; Lactoferrin; Lymphatic System; Muramidase; Plasma Cells