interleukin-8 and Dyspepsia

Even with the most effective treatment, Helicobacter pylori eradication is difficult in some patients. Therefore, patients sometimes require acid-suppressive therapy without H. pylori eradication. It has been reported that ranitidine inhibits neutrophil activation, whereas famotidine does not. However, few studies have been published concerning the activation of neutrophils before and after treatment using clinical doses of histamine-2 receptor antagonists in patients with H. pylori infection.. To examine the effects of neutrophil activation after treatment with three different histamine-2 receptor antagonists.. This prospective, open-label, randomised, parallel-group study was conducted. Thirty patients with H. pylori infection were enrolled. These subjects were randomly assigned to receive one of the following treatments: (a) 150 mg ranitidine, (b) 20mg famotidine, or (c) 10 mg lafutidine b.d., for 4 weeks. Before and after histamine-2 receptor antagonist treatment, histological findings, myeloperoxidase activity, and interleukin-8 in the gastric mucosa were evaluated.. On the basis of the histological findings between before and after histamine-2 receptor antagonist treatment, no significant differences were found in any groups. Similarly, there were no significant differences in myeloperoxidase activity or interleukin-8 levels.. In patients with H. pylori, when used at clinical doses, any histamine-2 receptor antagonists can be used without concerning about inhibition of neutrophil activation.

Topics: Acetamides; Adult; Dyspepsia; Famotidine; Female; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Interleukin-8; Male; Middle Aged; Neutrophil Activation; Peroxidase; Piperidines; Pyridines; Ranitidine

there are many determinant factors that may play roles in pathophysiology of functional dyspepsia. One of them is psychological stress that can increase plasma cortisol levels, alter inflammation process and affect Helicobacter pylori activity. No study has been conducted to find out the dominant factor among them. This study aimed to find the dominant factor among plasma cortisol levels, IL-6 and IL-8 expressions and H.Pylori activity, as the determinant factors in the pathophysiology of functional dyspepsia.. a cross-sectional study was conducted in 80 patients with dyspepsia syndrome at M. Djamil General Hospital, Padang, West Sumatera, Indonesia. The patients were categorized into two groups, i.e. the stress and non-stress group, which were identified using DASS 42 questionairre criteria. The inflammatory expressions (IL-6 and IL-8 expressions) as well as H. pylori activity were determined using immunohistochemistry of gastric biopsy specimens; while plasma cortisol levels was measured from peripheral blood samples. Data were analyzed using binary multivariate logistic regression.. there were 80 patients with functional dyspepsia with mean age of 38.9 years old. The morning cortisol levels was found significantly higher in the stress group. Higher IL-6 and IL-8 expressions were found in patients of non-stress group compared to those in the other group (IL-6: 73.28 (SD 16.60) vs. 72.95 (SD 19.49; and IL-8: 18.45 (SD 17.32) vs. 14.80 (SD 12.71)); although stastically not significant. There was greater Helicobacter pylori activity in the group with psychological stress compared to those in the non-stress group since there was antigen-antibody reaction invading the submucosa. The dominant determinant factor was the afternoon plasma cortisol levels.. many factors can become the determinant factors for gastric mucosal damage; however, our study has demonstrated that the dominant factor is afternoon plasma cortisol levels.

Topics: Adult; Cross-Sectional Studies; Dyspepsia; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Hydrocortisone; Immunohistochemistry; Indonesia; Interleukin-6; Interleukin-8; Logistic Models; Male; Middle Aged; Multivariate Analysis; Severity of Illness Index; Stress, Psychological

Helicobacter pylori (H. pylori) infection plays an important role in the carcinogenesis and development of gastric cancer. Eradication of H. pylori can effectively reduce the risk of gastric cancer, but the underlying mechanisms are not fully understood. This study aimed to investigate the effect of eradication of H. pylori on the expression levels of FHIT, IL-8 and P73 in the gastric mucosa of first-degree relatives of gastric cancer patients.. One hundred and thirty-two patients with functional dyspepsia having first-degree relatives with gastric cancer were prospectively recruited in this study. Nine patients presented with H. pylori infection and family histories of gastric cancer, 61 with H. pylori infection and without family histories of gastric cancer, 6 without H. pylori infection and with family histories of gastric cancer, and 56 without H. pylori infection and family histories of gastric cancer. The protein and mRNA expression levels of FHIT, IL-8 and P73 in gastric mucosa of the subjects were detected by immunohistochemical staining and polymerase chain reaction, respectively.. Compared with the patients without H. pylori infection and family histories of gastric cancer, both the protein and mRNA levels of FIHT significantly decreased in patients with H. pylori infection and/or family histories of gastric cancer, and both the protein and mRNA levels of IL-8 significantly increased. After eradication of H. pylori, both the protein and mRNA levels of FHIT were significantly higher, and both the protein and mRNA levels of IL-8 were significantly lower. However, H. pylori infection and family histories of gastric cancer had no major effect on P73 expression.. Down-regulation of FHIT and up-regulation of IL-8 may be involved in the pathogenesis of H. pylori infection in the first-degree relatives of gastric cancer patients.

Topics: Acid Anhydride Hydrolases; Adult; Aged; Anti-Bacterial Agents; Demography; DNA-Binding Proteins; Down-Regulation; Dyspepsia; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Interleukin-8; Male; Middle Aged; Neoplasm Proteins; Nuclear Proteins; Proton Pump Inhibitors; Real-Time Polymerase Chain Reaction; RNA, Messenger; Stomach Neoplasms; Tumor Protein p73; Tumor Suppressor Proteins; Up-Regulation

The envisaged roles and partly understood functional properties of Helicobacter pylori protein HP0986 are significant in the context of proinflammatory and or proapoptotic activities, the two important facilitators of pathogen survival and persistence. In addition, sequence analysis of this gene predicts a restriction endonuclease function which remained unknown thus far. To evaluate the role of HP0986 in gastric inflammation, we studied its expression profile using a large number of clinical isolates but a limited number of biopsies and patient sera. Also, we studied antigenic role of HP0986 in altering cytokine responses of human gastric epithelial (AGS) cells including its interaction with and localization within the AGS cells.. For in vitro expression study of HP0986, 110 H. pylori clinical isolates were cultured from patients with functional dyspepsia. For expression analysis by qRT PCR of HP0986, 10 gastric biopsy specimens were studied. HP0986 was also used to detect antibodies in patient sera. AGS cells were incubated with recombinant HP0986 to determine cytokine response and NF-κB activation. Transient transfection with HP0986 cloned in pEGFPN1 was used to study its subcellular localization or homing in AGS cells.. Out of 110 cultured H. pylori strains, 34 (31%) were positive for HP0986 and this observation was correlated with in vitro expression profiles. HP0986 mRNA was detected in 7 of the 10 biopsy specimens. Further, HP0986 induced IL-8 secretion in gastric epithelial cells in a dose and time-dependent manner via NF-κB pathway. Serum antibodies against HP0986 were positively associated with H. pylori positive patients. Transient transfection of AGS cells revealed both cytoplasmic and nuclear localization of HP0986.. HP0986 was moderately prevalent in clinical isolates and its expression profile in cultures and gastric biopsies points to its being naturally expressed. Collective observations including the induction of IL-8 via TNFR1 and NF-κB, subcellular localization, and seropositivity data point to a significant role of HP0986 in gastroduodenal inflammation. We propose to name the HP0986 gene/protein as 'TNFR1 interacting endonuclease A (TieA or tieA)'.

Topics: Antigens, Bacterial; Biopsy; Dyspepsia; Epithelial Cells; Female; Gene Expression Regulation, Bacterial; Helicobacter Infections; Helicobacter pylori; Host-Pathogen Interactions; Humans; Interleukin-8; Male; Middle Aged; NF-kappa B; Receptors, Tumor Necrosis Factor, Type I; Virulence Factors

Matrix metalloproteinases (MMPs) are endopeptidases which perform important functions in extracellular matrix remodeling, cell proliferation, and inflammatory processes. Here, we compared MMP-3 levels with those of tissue inhibitor of metalloproteinases (TIMP)-1 and several inflammatory cytokines in gastric ulcer (GU) patients.. This study enrolled 50 patients with GU and 6 with functional dyspepsia (FD). Samples of gastric mucosa from the antrum and the ulcer site were harvested from GU patients and of antral mucosa alone from FD patients during upper gastrointestinal endoscopy. Mucosal biopsy tissues were cultured for 24 h, and the culture supernatant was measured for levels of MMP-3, TIMP-1, IL-1beta, IL-6, and IL-8.. All GU patients were positive for Helicobacter pylori, while all FD patients were negative. Antral levels of TIMP-1, IL-1beta, IL-6, and IL-8 were significantly higher in GU than FD patients. Further, MMP-3 levels were significantly higher in GU patients at the ulcer site than in the antrum, and had a significantly positive correlation with TIMP-1, IL-1beta, IL-6, and IL-8.. MMP-3 levels were significantly higher at the ulcer site than in the antrum, suggesting that MMP-3 may perform an important function in gastric ulcer healing.

Topics: Adult; Aged; Aged, 80 and over; Dyspepsia; Endoscopy, Gastrointestinal; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-1; Interleukin-6; Interleukin-8; Linear Models; Male; Matrix Metalloproteinase 3; Middle Aged; Statistics, Nonparametric; Stomach Ulcer; Tissue Inhibitor of Metalloproteinase-1; Wound Healing

Helicobacter pylori (H. pylori) is a non-invasive microorganism causing intense gastric mucosal inflammatory and immune reaction. H. pylori-induced gastric mucosal cytokine overproduction has been clearly documented previously. The stomach has a large surface area and continuous spill-over of locally produced cytokines into the blood stream is a possibility. There are few and conflicting data on circulatory proinflammatory cytokine levels in patients with H. pylori infection.. Forty-two dyspeptic patients were enrolled into the study. The presence of H. pylori infection was diagnosed with antral histopathologic examination. After overnight fasting; serum samples were obtained from each patient to determine circulating interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha) levels.. H. pylori was shown in 30 cases using Giemsa stain in antral histopathologic evaluation. Twelve cases were negative for H. pylori staining. Both the age and sex distribution had an insignificant difference in both H pylori-positive and H. pylori-negative groups. The mean circulatory levels of IL-6, IL-8 and TNF-a in both groups were not different. The situation was same in respect to the serum levels of these cytokines and the degree of inflammation, H. pylori density and activation scores according to Sydney classification.. We could not show elevated circulatory levels of IL-6, IL-8 and TNF-alpha in H. pylori-infected cases. We believe that H. pylori-related cytokine activation become concentrated on gastric mucosa and this pathogen-induced local inflammatory cascade does not cause changes in circulatory levels of these cytokines. Moreover, there is no correlation between the levels of serum cytokines and Sydney parameters.

Topics: Adult; Cytokines; Dyspepsia; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation Mediators; Interleukin-6; Interleukin-8; Male; Middle Aged; Tumor Necrosis Factor-alpha

Isolates of Helicobacter pylori from dyspeptic patients in England and South Africa were tested for ability to induce interleukin-8 (IL-8) in gastric cells. All isolates were cagA-positive, which was used as a marker for the presence of the cag pathogenicity island. The aims were to determine if activities were related to diversity within cagE (HP0544), a locus encoding a key component in the Type IV secretion system, and if disease severity might be linked to a combination of strain features. We found that isolates were heterogeneous in ability to induce IL-8 activity with the 23 positive isolates (59%) showing activities ranging from 260 to 3200 pg ml(-1). The cagE locus was detected in most isolates and RFLP analysis of a 1.52-kb internal fragment showed interstrain diversity with 12 combined (MboI/NlaIII) types. Most cagE genotypes were not associated with IL-8 induction, however two genotypes were found only in IL-8-inducing strains and one genotype was associated with lack of IL-8 induction. IL-8 activity was not associated with either the number or composition of cagA tyrosine phosphorylation motifs and vacA m-type. Although we found a weak association between cagE type and the ability to induce IL-8, our results imply that gastric cell factors or bacterial factors other than vacA, cagA and cagE are involved in the induction of IL-8 and the development of severe gastric disease.

Topics: Antigens, Bacterial; Bacterial Proteins; Dyspepsia; Epithelial Cells; Gastric Mucosa; Gastrointestinal Diseases; Genetic Variation; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Phosphorylation; Severity of Illness Index; Tyrosine

Few reports exist on inflammation and interleukin (IL)-8 response in H. pylori-infected children. The aim of this study was to determine the intensity of inflammation, density of colonization and magnitude of IL-8 response in children with and without H. pylori infection.. We studied 45 children with dyspeptic symptoms, 21 infected with H. pylori and 24 without infection. Antrum and corpus gastric biopsies were obtained and studied for H. pylori infection with an immunofluorescence technique and for IL-8 with an immunohistochemical assay. Biopsy specimens were stained with hematoxilin and eosin and gastritis was graded according to the Sydney system. The magnitudes of the IL-8 response and H. pylori colonization were estimated microscopically with image analyzer software.. In H. pylori-infected children, mild mono-nuclear cell infiltration was found in 50%, and no neutrophils in 40% of cases. In the antrum but not in the corpus, the intensity of colonization correlated with neutrophil and mononuclear cell infiltration. The IL-8 response was significantly higher in the antrum (p <.05) and corpus (p <.02) of infected children, and was localized mainly in the surface and crypts of the epithelium. No correlation was found between the magnitude of the IL-8 response and the infiltration of either neutrophil or mononuclear cells.. In H. pylori-infected children, poor mononuclear and neutrophil infiltration was observed. Infection was associated with a higher IL-8 response by gastric epithelial cells. The density of colonization but not the IL-8 response correlated with neutrophil cell infiltration.

Topics: Adolescent; Child; Dyspepsia; Epithelial Cells; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Leukocytes, Mononuclear; Male; Neutrophil Infiltration

Helicobacter pylori infection is associated with a variety of outcomes ranging from seemingly asymptomatic coexistence to peptic ulcer disease and gastric cancer. The cag pathogenicity island (PAI) contains genes associated with a more aggressive phenotype and has been suggested to be a determinant of severe disease outcome. The cagA gene has served as a marker for the cag PAI. However, the presence of this single gene does not necessarily indicate the presence of a complete set of cag PAI genes. We have analyzed the composition of the cag PAI in 66 clinical isolates obtained from patients with duodenal ulcer, gastric cancer, and nonulcer dyspepsia. Hybridization of DNA to microarrays containing all the genes of the cag PAI showed that 76 and 9% of the strains contained all or none of the cag PAI genes, respectively. Partial deletions of the cag PAI were found in 10 isolates (15%), of which 3 were cagA negative. The ability to induce interleukin-8 (IL-8) production in AGS cells was correlated to the presence of a complete cag PAI. Strains carrying only parts of the island induced IL-8 at levels significantly lower than those induced by cag PAI-positive isolates. The presence of an intact cag PAI correlates with development of more severe pathology, and such strains were found more frequently in patients with severe gastroduodenal disease (odds ratio, 5.13; 95% confidence interval, 1.5 to 17.4). Partial deletions of the cag PAI appear to be sufficient to render the organism less pathogenic.

Topics: Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Base Sequence; Duodenal Ulcer; Dyspepsia; Helicobacter pylori; Humans; Interleukin-8; Molecular Sequence Data; Oligonucleotide Array Sequence Analysis; Stomach Neoplasms

Despite numerous epidemiological studies, the association between Helicobacter pylori infection and gastric cancer (GC) remains unexplained. This study was designed to determine the seropositivity of H. pylori and cytotoxin-associated gene A (CagA), serum gastrin and interleukin-8 (IL-8) levels as well as basal intragastric pH and maximal histamine-induced gastric acid outputs (MAO) in a large series of GC patients and controls.. 337 GC patients (118 men and 219 women; median age 59.4; range 21-87) and 337 controls randomized for sex and age entered the study. Serum IgG antibodies to H. pylori and CagA and serum levels of IL-8 were measured by enzyme-linked immunosorbent assay, while serum-amidated gastrin was determined by specific radioimmunoassay and correlated with gastric luminal pH.. The numbers of GC patients and controls involved in the study in various age groups, ranging from 20 to > 70 years, were similar, but overall H. pylori IgG seropositivity in GC patients was significantly higher (90.8%) than in controls (79.2%). The overall CagA seropositivity in GC patients was about double (58.2%) that in controls (25.2%). Serum gastrin levels over the calculated cut-off value (38.88 pM/L) were found in several-fold larger number in GC patients (48%) than in controls (8.3%) and. similarly, serum IL-8 values over the cut-off point (1.77 pg/mL) occurred in almost all (99.7%) GC patients but in only a few controls (0.3%). Basal intragastric pH above the cut-off point (pH = 4.50) was observed in about 58.2% of GC patients compared to 15.1% in controls, and strong correlation between the serum gastrin and gastric pH was found in GC but weak in controls. The cut-off value for MAO was 12.3 mml/h; MAO below this cut-off value occurred in 89.9% of GC patients and in only 4.7% of controls. A summary odds ratio (SOR) in GC for H. pylori IgG was 2.59 (95% Cl: 1.61-4.22) for CagA - 4.12 (95% Cl; 2.93-5.8), for serum gastrin - 10.25 (95%; 6.47-16.47) and for MAO - 15.2 (95% Cl; 9.45-39.82). Multivariable analysis of serum gastrin, IgG and CagA, and luminal pH and MAO values revealed that only gastrin and CagA have significant influence on GC formation (OR > 1 in logistic regression).. 1. CG patients show significantly higher H. pylori IgG and CagA seropositivity than dyspeptic age- and gender-matched controls, confirming that gastric infection with CagA expressing H. pylori greatly increases the risk of GC. 2. Serum gastrin levels in GC but not in controls are correlated with the rise in intragastric pH, indicating that excessive gastrin release in GC is affected by lower intragastric pH. 3. Serum gastrin level and CagA seropositivity are significantly increased in the majority of GC patients, and are the only variables in multivariable analysis to have a predominant influence on GC formation, which suggests that both these parameters may be implicated in H. pylori-related gastric carcinogenesis. 4. H. pylori-infected GC patients produce significantly more IL-8 than do non-GC controls, probably reflecting CagA-positive H. pylori-associated gastritis.

Topics: Adult; Aged; Aged, 80 and over; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Dyspepsia; Enzyme-Linked Immunosorbent Assay; Female; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Interleukin-8; Male; Middle Aged; Radioimmunoassay; Stomach Neoplasms

Chemokines that play a primary role in active inflammation are increased in gastric mucosa infected with Helicobacter pylori. Cigarette smoking increases the risk of peptic ulcer disease and gastric cancer, whereas alcohol might exert an antibacterial role. The aim of this study was to examine the association between smoking or alcohol consumption and mucosal chemokine mRNA expression in H pylori associated gastritis.. Gastric biopsy specimens were obtained from 46 patients with dyspepsia who were infected with H pylori, and total RNA was extracted. Semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed to quantify the mRNA expression of three C-X-C chemokines (interleukin 8 (IL-8), growth related oncogene alpha (GRO alpha), epithelial neutrophil activating protein 78 (ENA-78)) and two C-C chemokines (regulated on activation normal T cell expressed and secreted (RANTES) and monocyte chemotactic protein 1 (MCP-1)).. GRO alpha and ENA-78 mRNA expression was significantly increased (p < 0.05) in 22 smokers compared with 24 non-smokers; however, no difference was seen in the expression of IL-8, RANTES, and MCP-1 mRNA. No differences were observed in chemokine mRNA expression in relation to alcohol consumption.. The increased C-X-C chemokine mRNA expression seen in smokers might play a role in inducing enhanced inflammatory activity in gastritis and the consequent severe diseases associated with H pylori infection.

Topics: Alcohol Drinking; Case-Control Studies; Chemokine CCL2; Chemokine CCL5; Chemokine CXCL1; Chemokine CXCL5; Chemokines; Chemokines, CXC; Chemotactic Factors; Chi-Square Distribution; Dyspepsia; Gastric Mucosa; Growth Substances; Helicobacter Infections; Helicobacter pylori; Humans; Intercellular Signaling Peptides and Proteins; Interleukin-8; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Smoking

Helicobacter pylori infection is the commonest cause of gastritis. Different patterns of immune response to H. pylori infection and characteristics of bacteria are considered to contribute to clinical outcomes.. To determine characteristics of the host H. pylori relationship in subjects with non-ulcer dyspepsia and a histological diagnosis of gastritis.. Thirty-five subjects with chronic gastritis undergoing endoscopy (mean age 53 years, range 24-82, 14 male and 21 female) were studied, none of whom was on nonsteroidal anti-inflammatory drugs or antibiotics. H. pylori infection was determined by rapid urease test (CLOtest), culture, antibody and RT-PCR for Ure C, Cag A and 26 kDa gene and histology. Cytokine production of mucosal IL-6 and IL-8 were measured by ELISA.. Fifteen subjects were positive by CLOtest and/or bacterial culture. In these subjects histology showed numerous helical forms of H. pylori (Group I). Nine subjects were negative by CLOtest, bacterial culture, and mRNA for urease C fragment, but positive by PCR for the 26 kDa protein encoding gene. Histology in these subjects showed the presence of either coccoid forms (four), or scant helical forms (two), or mixed coccoid/helical forms (three) (Group II). Eleven subjects were negative by all methods of detection (Group III). IgG and IgA antibody levels in serum (p<0.05) and gastric tissue culture supernatant (p<0.001) were significantly higher in Group I than those in Group II or III. There were significant differences in the IgG serum and IgA supernatant antibody levels (p<0.01 and p<0.05) when Group II was compared to Group III. Supernatant IL-6 levels were significantly higher in Group I (p<0.01) than those from Groups II and III. IL-8 levels were higher in Group I (p<0.01) and Group II (p<0.05) when compared to Group III.. 'H. pylori-negative' gastritis can be associated with a non-urease producing form of H. pylori, with a reduction in both local and systemic antibody levels and mucosal pro-inflammatory cytokines.

Topics: Adult; Aged; Aged, 80 and over; Chronic Disease; Dyspepsia; Enzyme-Linked Immunosorbent Assay; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin A; Immunoglobulin G; Interleukin-6; Interleukin-8; Male; Middle Aged; Polymerase Chain Reaction; Urease

Mucosal IgA is important in local immune defence. Helicobacter pylori induces a specific IgA response in antral mucosa, but its immunopathology is unknown. Interleukin-8 (IL-8) has been suggested to be important in H. pylori-induced inflammation. Current information on the relationship between H. pylori-induced IgA and mucosal inflammation is limited. To investigate possible associations between mucosal-specific IgA, the toxinogenicity of H. pylori, mucosal levels of IL-8 and gastric inflammation, 52 endoscoped patients were studied. These comprised 28 patients with peptic ulcer and 24 with non-ulcer dyspepsia. Of these patients, 38 had H. pylori infection: 28 with peptic ulcer and 10 with non-ulcer dyspepsia. Antral biopsies were taken for histology, H. pylori culture and measurement of mucosal levels of IL-8 (pg/mg) and specific IgA (A450x1000) by ELISA. Mucosal H. pylori IgA was detectable in 35 out of 38 patients with H. pylori infection, with a median (interquartile) level of 220 (147, 531) units. There was no significant difference in mucosal levels of the IgA antibodies between patients infected with cytotoxin-positive or cagA-positive strains of H. pylori and those with toxin-negative or cagA-negative strains. The IgA levels in those patients with severe neutrophil infiltration were lower than in those with mild or moderate infiltration (P<0.05). There was a weak inverse correlation between antral mucosal IgA and IL-8 in infected patients (r=-0.36; P=0.04). H. pylori infection induced a significant local mucosal IgA response in most infected patients. The level of IgA antibodies does not appear to be correlated with the toxinogenicity of H. pylori. However, patients with severe active inflammation appear to have decreased levels of IgA. An inverse correlation between mucosal IL-8 and IgA may suggest that IL-8-induced inflammation compromises the mucosal IgA defence and renders the mucosa susceptible to further damage.

Topics: Adult; Antibodies, Bacterial; Antigens, Bacterial; Bacterial Proteins; Dyspepsia; Female; Gastric Mucosa; Gastritis; Gastroscopy; Helicobacter pylori; Humans; Immunity, Mucosal; Immunoglobulin A; Interleukin-8; Male; Middle Aged; Peptic Ulcer; Polymerase Chain Reaction; Statistics, Nonparametric

Helicobacter pylori strains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8.. To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA).. In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1 beta, IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor alpha (TNF-alpha) in antral biopsy specimens were measured by ELISA.. Mucosal levels of IL-1 beta, IL-6, IL-8, and TNF-alpha were significantly higher in H pylori positive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1 beta and IL-8 were significantly higher in specimens infected with cagA positive strains than in those infected with cagA negative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1 beta (p < 0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-alpha (p < 0.0001).. These findings suggest that the ability to induce cytokines differs among the strains; cagA+ strains induce various kinds of cytokines and may cause severe inflammation, whereas cagA- strains induce IL-8 and IL-1 beta only weakly and may cause only mild inflammation. However, as most patients infected with the cagA+ strains have gastritis, these strains may not be equivalent to ulcerogenic strains.

Topics: Adult; Aged; Aged, 80 and over; Antigens, Bacterial; Bacterial Proteins; Colony Count, Microbial; Cytokines; Dyspepsia; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastritis; Genes, Bacterial; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-1; Interleukin-6; Interleukin-8; Male; Middle Aged; Polymerase Chain Reaction; Tumor Necrosis Factor-alpha

To determine the mechanisms of gastric mucosal injury associated with Helicobacter pylori infection, we investigated the contents of cytokines and inflammatory cell infiltration in the gastric mucosa. Ninety-six patients with dyspepsia were studied (58 gastric ulcer, 38 nonulcer dyspepsia). Of the 96 patients, 63 were infected with H. pylori as determined by microscopic examination with HE staining, culture of H. pylori, or the rapid urease test. Endoscopic biopsy specimens were obtained from both the antrum and the body to examine interleukin (IL)-8, IL-6, IL-1 beta, and tumor necrosis factor-alpha contents in the gastric mucosa by enzyme-linked immunosorbent assay. Inflammatory cell infiltration was assessed according to the Sydney system. IL-8 content was enhanced in both the antral and body mucosa of the H. pylori-positive patients compared with the H. pylori-negative patients. Furthermore, IL-8 content correlated well with the infiltration of both mononuclear cells and polymorphonuclear cells. These results suggest that IL-8 plays important roles in the pathogenesis of gastric mucosal injury associated with H. pylori infection.

Topics: Case-Control Studies; Cytokines; Dyspepsia; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Male; Middle Aged; Stomach Ulcer

To investigate the role of interleukin-8 (IL-8) and tumour necrosis factor (TNF) in patients infected with Helicobacter pylori.. The study population comprised 52 patients with dyspepsia attending for upper gastrointestinal endoscopy. Of these patients, 35 were infected with H pylori. IL-8 and TNF concentrations in plasma, gastric juice, and gastric biopsy homogenate supernatant fluid were measured by radioimmunoassay and L929 cell bioassay, respectively.. The concentrations of IL-8 and TNF in gastric juice and gastric biopsy homogenates were substantially greater in patients infected with H pylori. In H pylori positive patients IL-8 concentrations in gastric juice and gastric biopsy homogenates were higher in those with moderate gastritis than in those with mild gastritis. There was a positive correlation between IL-8 and TNF concentrations in gastric juice and gastric biopsy homogenate supernatant fluid from H pylori positive patients. There were no significant differences between H pylori positive and negative patients with respect to IL-8 and TNF plasma concentrations.. This study suggests that increased gastric production of IL-8 and TNF may be implicated in the pathogenesis of H pylori associated gastroduodenal disease.

Topics: Adult; Aged; Biological Assay; Cytokines; Dyspepsia; Female; Gastric Juice; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Male; Middle Aged; Tumor Necrosis Factor-alpha

To determine the concentrations of interleukin-1 beta, interleukin-6, and interleukin-8 in tissue homogenates of mucosal biopsy specimens from Helicobacter pylori-positive and -negative patients.. In 43 consecutive patients who underwent upper gastrointestinal endoscopy, seven antral biopsies were taken; three specimens were used for cytokine determination and the remaining four biopsies were processed for H. pylori detection. Peripheral venous blood was collected and IgG to H. pylori was assayed by an ELISA technique.. Twenty-nine of 43 patients (67%) were histologically positive for H. pylori; all had chronic gastritis. The mucosal levels of interleukin-6 and interleukin-8 were significantly higher in H. pylori-positive patients than in the negative patients (p < 0.001). A significantly higher percentage of interleukin-8 was found in patients colonized by H. pylori with active superficial chronic gastritis (85.7%), compared to quiescent superficial gastritis (12.5%) (p < 0.01), and the median and range were, respectively, 400 (0-1000) and 0 (0-200) pg/mg protein (p < 0.001). In patients with active superficial gastritis, a significant correlation between interleukin-6 and -8 was found (p 0.01). No difference was found regarding the mucosal levels of interleukin-1 beta according to the presence of H. pylori.. These results suggest a possible pathogenetic role for interleukin-6 and interleukin-8 in H. pylori-associated gastritis.

Topics: Adult; Aged; Chronic Disease; Dyspepsia; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-6; Interleukin-8; Male; Middle Aged