muramidase and Gastritis

The mucosa of the esophagus, the stomach, the small intestine, the large intestine and rectum are unremittingly challenged by adverse micro-environmental factors, such as ingested pathogenic and non-pathogenic bacteria, and harsh secretions with digestive properties with disparate pH, as well as bacteria and secretions from upstream GI organs. Despite the apparently inauspicious mixture of secretions and bacteria, the normal GI mucosa retains a healthy state of cell renewal. To by-pass the tough microenvironment, the epithelia of the GI react by speeding-up cell exfoliation, by increasing peristalsis, eliminating bacteria through secretion of plasma cell-immunoglobulins and by increasing production of natural antibacterial enzymes (lysozyme) and host defense peptides (defensin-5). Lysozyme was recently found up-regulated in Barrett's esophagitis, in chronic gastritis, in gluten-induced atrophic duodenitis (celiac disease), in collagenous colitis, in lymphocytic colitis and in Crohn's colitis. This up-regulation is a response directed towards the special types of bacteria thriving in the microenvironment in each of the aforementioned clinical inflammatory maladies. The purpose of that up-regulation is to protect the mucosa affected by the ongoing chronic inflammation. Bacterial antibiotic resistance continues to exhaust our supply of effective antibiotics. The future challenge is how to solve the increasing menace of bacterial resistance to anti-bacterial drugs. Further research on natural anti-bacterial enzymes such as lysozyme, appears mandatory.

Topics: Barrett Esophagus; Celiac Disease; Colitis, Collagenous; Colitis, Lymphocytic; Colitis, Ulcerative; Crohn Disease; Gastritis; Gastrointestinal Diseases; Humans; Inflammation; Muramidase

Topics: Acid Phosphatase; Alkaline Phosphatase; Amylases; Carbonic Anhydrases; Chronic Disease; Gastric Juice; Gastric Mucosa; Gastritis; Glucuronidase; Humans; Leucyl Aminopeptidase; Lipase; Muramidase; Oxidoreductases; Peptide Hydrolases

The article presents findings allowing estimating effect of local application of polioxidonium and yantum verde in 101 children aged 12-17 with chronic catarrhal gingivitis and chronic gastroduodenitis. Statistically significant PMA indeх decrease (40.1±2.3% till 1.4±0.6% (р<0,001)) proved the above mentioned therapy scheme to be highly effective for treatment of chronic catarrhal gingivitis in children with chronic gastroduodenitis.

Topics: Adolescent; Anti-Inflammatory Agents, Non-Steroidal; Benzydamine; Child; Chronic Disease; Drug Therapy, Combination; Duodenitis; Female; Gastritis; Gingivitis; Humans; Immunoglobulin A; Immunoglobulin A, Secretory; Immunoglobulin G; Immunologic Factors; Interleukin-10; Interleukin-1beta; Male; Mouth; Muramidase; Piperazines; Polymers; Saliva

Systemic amyloidoses is a heterogeneous group of diseases either acquired or hereditary. Amyloidoses can involve the gastrointestinal tract and the nature of the precursor protein that forms the fibrils deposits should be identified to adjust the treatment and evaluate the prognosis. Lysozyme amyloidosis (ALys) is a rare, systemic non neuropathic hereditary amyloidosis with a heterogenous phenotype including gastrointestinal, renal and hepatic symptoms.. We report and describe symptoms and gastrointestinal tract involvement in a new family with hereditary lysozyme amyloidosis. Clinical manifestations and organ involvement of nine affected members of a new family with the p.Trp82Arg ALys variant were recorded. All affected individuals suffered with prevailing gastrointestinal symptoms leading to the diagnosis of ALys. 8/9 had non specific upper gastrointestinal symptoms and 3/9 had rectocolic inflammation evoking inflammatory bowel disease. No other organ involvement by amyloidosis was found. Histological examination revealed amyloid deposits in all cases and all carried the p.Trp82Arg ALys variant at a heterozygous state.. Hereditary amyloidosis associated with the p.Trp82Arg lysozyme variant in this new family is predominantly associated with mild upper gastrointestinal tract involvement and in some cases with inflammatory bowel disease. Amyloidosis should be considered in atypical or treatment resistant, upper or lower chronic gastrointestinal symptoms. When associated with a familial history a lysozyme gene mutation must be searched.

Topics: Adult; Aged; Amyloidosis, Familial; Female; Gastritis; Humans; Inflammatory Bowel Diseases; Male; Middle Aged; Muramidase; Mutation; Pedigree; Phenotype; Young Adult

Backgroud: Helicobacter pylori (Hp) rarely proliferates in patients with fundic gland polyps (FGPs). We recently found that FGPs express lysozyme, one of the natural defence substances against infection. We aimed to assess the degree of lysozyme expression in a cohort of consecutive FGPs.. A total of 153 gastric biopsies were investigated: 93 with FGPs, 30 with normal mucosa (Nm), 15 with Hp-induced chronic gastritis (Hp-gastritis) and 15 with chronic gastritis without Hp infection (non-Hp-gastritis). Sections were stained with anti-lysozyme (muramidase).. Lysozyme was slightly to moderately expressed in the surface and foveolar pits, being markedly expressed in the neck glands in Nm, in non-Hp and Hp-gastritis. The ratio of lysozyme neck glands-foveoli was higher in non-Hp than in Nm and even higher in Hp-gastritis. In FGPs, lysozyme was markedly expressed in the surface, the foveolar pits and the cells that partly or entirely covered the microcysts.. While the moderate expansion of the lysozyme-producing cells of the neck glands in Hp-gastritis might be insufficient to eradicate these bacteria, the overproduction of lysozyme in the epithelium covering FGP could be an explanation for the lack of Hp proliferation in these patients.

Topics: Biopsy; Chronic Disease; Gastric Fundus; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Muramidase; Polyps; Stomach Diseases

The increase in the transcellular passage of intact antigens across the digestive epithelium infected with Helicobacter pylori may interfere with the regulation of mucosal immune responses. The aim of this work was to study the capacity of Helicobacter infection to inhibit the development of oral tolerance or to promote allergic sensitization and the capacity of a gastro-protective agent, rebamipide, to interfere with these processes in mice. Oral tolerance to ovalbumin (OVA) was studied in 48 C3H/He 4-week-old mice divided into four groups: (i) OVA-sensitized mice; (ii) OVA-"tolerized" mice (that is, mice that were rendered immunologically tolerant); (iii) H. felis-infected, OVA-tolerized mice; (iv) and H. felis-infected, OVA-tolerized, rebamipide-treated mice. Oral sensitization to hen egg lysozyme (HEL) was studied in 48 mice divided into four groups: (i) controls; (ii) HEL-sensitized mice; (iii) H. felis-infected, HEL-sensitized mice; and (iv) H. felis-infected, HEL-sensitized, rebamipide-treated mice. Specific anti-OVA or anti-HEL immunoglobulin E (IgE) and IgG1/IgG2a serum titers were measured by enzyme-linked immunosorbent assay. Additionally, the capacity of rebamipide to interfere with antigen presentation and T-cell activation in vitro, as well as absorption of rebamipide across the epithelial monolayer, was tested. H. felis infection led to the inhibition of oral tolerance to OVA, but rebamipide prevented this inhibitive effect of H. felis. H. felis infection did not enhance the sensitization to HEL, but rebamipide inhibited the development of this sensitization. Moreover, rebamipide inhibited in a dose-dependent manner antigen presentation and T-cell activation in vitro and was shown to be able to cross the epithelium at a concentration capable of inducing this inhibitory effect. We conclude that H. felis can inhibit the development of oral tolerance to OVA in mice and that this inhibition is prevented by rebamipide.

Topics: Administration, Oral; Alanine; Anaphylaxis; Animals; Antigen Presentation; Antigens; Chickens; Female; Gastritis; Helicobacter Infections; Immune Tolerance; Immunity, Mucosal; Immunoglobulin E; Immunoglobulin G; In Vitro Techniques; Intestines; Mice; Mice, Inbred C3H; Muramidase; Ovalbumin; Quinolones; T-Lymphocytes

To investigate aggressive-protective factors in patients with erosive lesions of gastroduodenal mucosa.. Intragastric pH-metry, tests for Helicobacter pylori, lysozyme activity, content of bile acid in gastric juice, components of gastric mucous gel were made in 106 patients.. It is shown that there are two alternative paths of erosions development in the gastroduodenal zone: infectious and non-infectious.. In patients infected with Helicobacter pylori, lowering of a protective ability of the mucous gel is caused by prevalence of synthesis of immature mucous components while in non-infected patients this happens as a result of high catabolism of mucous components.

Topics: Adult; Bile Acids and Salts; Duodenal Ulcer; Duodenitis; Gastric Juice; Gastric Mucosa; Gastritis; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Intestinal Mucosa; Middle Aged; Mucus; Muramidase; Peptic Ulcer; Stomach Ulcer

Granulocyte infiltration was studied in 88 biopsies of antrum mucosa from patients with B-gastritis. Evidence of IgA-, IgG- and IgM-antibodies as well as of lysozyme in the mucosa was demonstrated by immunohistochemical methods. Helicobacter pylori (Hp) is coated by antibodies and a significant correlation between extent of opsonisation and number of plasma cells in the connective tissue of the lamina propria could be stated. Thus, the infiltration of plasma cells is a specific immune response against Hp. In the depths of gastric pits the antibody-coating of bacteria is faint. Instead, lysozyme and lactoferrin are produced there. By means of a Cross-sectional study a model is developed which characterizes B-gastritis as a dynamic process. Lagging behind, the inflammation follows the motile bacteria resulting in a patchy distribution of inflamed areas in the mucosa. At the peak of these local inflammation-waves the production of antibodies and lysozyme is intensified. Coating the bacteria with IgG and IgM results in complement activation liberating chemotaxin C5a. Consequently, there is a massive granulocyte infiltration leading to local reduction or eradication of Hp.

Topics: Antibodies, Bacterial; Antibody Specificity; Biopsy; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoenzyme Techniques; Immunoglobulins; Muramidase

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

A total of 238 randomly selected gastric biopsies were examined with polyclonal antibodies from rabbits (antihuman-lysozyme and antihuman-lactoferrin) using the Peroxidase-Antiperoxidase-method according to Sternberger. The preparations were evaluated by comparing the intensity of the staining as well as the quantity and distribution of positive cells within the mucosa. The results show that lysozyme can be demonstrated constantly in the glandular neck zone and in the mucoid glandular body within the normal non-inflamed mucosa of the antrum, whereas in the normal corpus mucosa only a small amount of lysozyme appears focally and inconsistently in the neck area of the glands. A substantial increase in the intensity of lysozyme presentation due to inflammatory changes as related to the chronic superficial gastritis of the antrum cannot be discovered. On the contrary, the presentable amount of lysozyme decreases in line with the progressing inflammation and, in case of chronic-atrophic gastritis with intestinal metaplasia is restricted to the Paneth cells. A distinct and constant presentation of lysozyme can be achieved in the glandular neck zone, in the lower gastric pits and partially in the upper glandular body of the corpus mucosa in cases of chronic inflammatory processes. Obviously lysozyme is formed in the epithelial cells and not taken up from other cells. Furthermore it can be concluded from the findings that to a large extent lysozyme formation is linked to the proliferation activity of the epithelial cells. Lactoferrin cannot be found in normal non-inflammatory mucosa neither of the antrum nor of the corpus. But it can be found among most of the biopsy specimens with inflammatory changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Biopsy; Campylobacter Infections; Female; Gastric Mucosa; Gastritis; Gastritis, Atrophic; Granulocytes; Humans; Immunoenzyme Techniques; Lactoferrin; Lactoglobulins; Male; Metaplasia; Middle Aged; Muramidase

Indices of unspecific resistance (bactericidal serum activity, phagocytic reaction of neutrophils, lysozyme) were examined in 128 patients with ulcer disease and chronic gastritis. Changes of local and general mechanisms of unspecific reactivity of the gastro-intestinal tract result not only in disorders of the defence system but also in a reduction of viability of the gastric and duodenal epithelium with development of alteration processes. In this condition bacterial and protein antigens may change the immunological status of the body.

Topics: Blood Bactericidal Activity; Chronic Disease; Gastric Juice; Gastritis; Humans; Immunity, Innate; Muramidase; Peptic Ulcer; Phagocytosis

Biopsy specimens from Billroth-II-resected stomachs obtained endoscopically 28-32 years after the operation were subjected to an immunohistochemical study by two-colour immunofluorescence staining. The epithelial distribution of immunoglobulin A (IgA), secretory component (SC), lysozyme (Ly), and lactoferrin (Lf) was evaluated, and IgA-, IgM-, and IgG-producing cells were quantified in the lamina propria. Gastric body mucosa excised from resected stomachs obtained from patients with duodenal ulcer was used as control and showed considerably less extensive gastritis than the stump mucosa. Both specimen categories showed enhanced expression of epithelial IgA, SC, Ly, and Lf associated with severe gastritis, except for areas with intestinal metaplasia, which lacked Ly and Lf. The number of IgA-, IgM-, and IgG-producing cells was significantly increased with increasing degree of gastritis, particularly so for IgG cells on a relative basis. After partial gastrectomy, therefore, the stump mucosa generally responds with activation of local immune mechanisms; this response is principally similar to that seen in simple gastritis of comparable severity.

Topics: Adult; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastritis; Gastroscopy; Humans; Immunoglobulin A; Lactoferrin; Male; Middle Aged; Muramidase; Stomach; Time Factors

Topics: Adolescent; Biliary Dyskinesia; Child; Child, Preschool; Duodenitis; Gastric Juice; Gastritis; Humans; Immunoglobulins; Muramidase; Oropharynx; Pancreatitis; Saliva

We examined the infiltration in chronic superficial gastritis immunohistochemically on the contents of IgA-, IgG- and IgM-containing plasma cells and on lysozyme and compared the results on the one hand with those of histologically normal gastric mucosa and on the other side with those of the inflammation at the ulcus border. Not as immunology-related reactions of the gut, one can see the chronic superficial gastritis as a stronger and topographically different variant of the normal reaction of the stomach. It shows the flowing threshold between physiological and accentuated defense and pathological exaggeration.

Topics: Chronic Disease; Epithelium; Gastric Mucosa; Gastritis; Humans; Immunoenzyme Techniques; Immunoglobulins; Muramidase; Plasma Cells; Stomach Ulcer

Topics: Adolescent; Antibody Formation; Child; Chronic Disease; Duodenitis; Gastric Juice; Gastritis; Humans; Immunity, Innate; Mucins; Muramidase

Epithelial distributions of immunoglobulin A, secretory component, lysozyme, and lactoferrin were studied by paired immunofluorescence staining in ethanol-fixed biopsy specimens from gastric antral and body mucosa. Fluorescence scores were assigned semiquantitatively for the epithelium in three mucosal zones (foveolar, isthmus, and glandular). In each case, degree of inflammation was graded blindly after conventional histologic staining of serial sections. The results showed that the overall epithelial expression of local defense factors was significantly enhanced in association with gastritis, both with regard to nonspecific antimicrobial substances (lysozyme and lactoferrin) and the external transfer of immunoglobulin A (mediated by secretory component) as a potential carrier of protective antibodies. The antral isthmus and glandular zones were most active in both respects. Despite the expression of relatively large amounts of epithelial immunoglobulin A and secretory component in metaplastic glands, these elements lacked the nonspecific defense factors (except for lysozyme in Paneth cells)--even when they occurred in the antral mucosa--and may, therefore, represent particularly vulnerable areas.

Topics: Adult; Aged; Female; Fluorescent Antibody Technique; Gastric Mucosa; Gastritis; Humans; Immunoglobulin A; Immunoglobulin G; Immunoglobulin M; Immunoglobulins; Lactoferrin; Lactoglobulins; Male; Metaplasia; Middle Aged; Muramidase; Secretory Component; Staining and Labeling

Topics: Child; Child, Preschool; Chronic Disease; Duodenitis; Duodenum; Female; Gastritis; Humans; Immunoglobulins; Intestinal Secretions; Male; Muramidase

Serum lysozyme was reevaluated in inflammatory bowel disease and other gastrointestinal disorders. A total of 109 patients were divided into six groups: ulcerative colitis (28), Crohn's disease (9), simple atrophic gastritis (16), atrophic gastritis and pernicious anemia (23), functional dyspepsia (17), and controls (16). Elevated levels of lysozyme, compared with control levels, were found not only in ulcerative colitis and Crohn's disease but also in atrophic gastritis with or without pernicious anemia and in functional dyspepsia. The elevation of lysozyme, since it results from the product of granulocytes and macrophages present in increased amounts in the mucosa of inflammatory bowel diseases, is easily explained. The cellular infiltration in atrophic gastritis may also explain the elevated lysozyme levels. The higher lysozyme levels in some patients with functional dyspepsia could possibly reflect an underlying latent inflammatory process.

Topics: Adult; Aged; Anemia, Pernicious; Colitis, Ulcerative; Crohn Disease; Dyspepsia; Female; Gastritis; Humans; Male; Middle Aged; Muramidase

Using an immunoperoxidase technique the distribution of secretory component, IgA, and lysozyme has been investigated in normal, inflamed, dysplastic, and carcinomatous gastric mucosa. Apart from pyloric glands which contain lysozyme, normal gastric mucosa stains negatively for all three antigens. In gastric mucosa neck cells appear to adapt by synthesising secretory component and lysozyme and transporting IgA. Intense staining for the three antigens is seen in dysplastic gastric epithelium and in well-differentiated intestinal type carcinomas. With progressive de-differentiation the tumours lose the ability to synthesise secretory component and lysozyme. Carcinomas of the diffuse type stain positively for secretory component and lysozyme and individual cells appear to take up IgA even in the absence of surrounding IgA containing plasma cells. These functional properties are retained in lymph node metastases. It is suggested that secretory component synthesising malignant cells might take up circulating dimeric IgA and that this could be a reflection of an important physiological mechanism.

Topics: Gastric Mucosa; Gastritis; Humans; Immunoenzyme Techniques; Immunoglobulin A; Immunoglobulin Fragments; Muramidase; Secretory Component; Stomach Diseases; Stomach Neoplasms

No microbial growth in platings of the gastric juice of patients with gastric ulcer and chronic anacidic gastritis was observed. It means that the absence of hydrochloric acid in the gastric juice does not deprive it of any antimicrobial action. The possible role of lysozyme in providing sterility of the proximal part of the gastro-intestinal tract was studied. Eighty patients with chronic diseases of the digestive organs were observed. It was noted that the levels of lysozyme in the gastric juice was high and markedly exceeded the maximum concentrations required for lysis of organisms most resistant to it. The maximum concentration was determined at pH of the gastric juice equal to 7.0-7.5 (265 gamma/ml+/-28). No lysozyme in the content of the duodenum and jejunal juice was found in most cases. Its presence in the above parts of the gastro-intestinal tract was mainly associated with microbial growth. The maximum concentration of lysozyme (40 gamma/ml) in the jejunal juice was observed in a female patient with chronic enterocolitis and significant microbial proliferation in the thin colon (more than 10(4) microbial bodies per 1 ml of the juice). Such parallelism between the presence of lysozyme in the gastric juice and microbial proliferation in it may be considered as a protective-adoptive reaction of the host.

Topics: Chronic Disease; Enterocolitis, Pseudomembranous; Gastric Juice; Gastritis; Hepatitis; Humans; Intestinal Secretions; Intestine, Small; Muramidase; Pancreatitis; Postgastrectomy Syndromes; Sterilization; Stomach Ulcer

Topics: Colitis, Ulcerative; Gastric Mucosa; Gastritis; Humans; Immunoglobulins; In Vitro Techniques; Intestinal Mucosa; Muramidase

Topics: Chronic Disease; Gastric Mucosa; Gastritis; Humans; Muramidase; Peptic Ulcer

Topics: Animals; Appendicitis; Biological Evolution; Cell Division; Colitis, Ulcerative; Colonic Neoplasms; Crohn Disease; Ethionine; Gastritis; Germ-Free Life; Histocytochemistry; Humans; Intestinal Neoplasms; Intestines; Metaplasia; Microscopy, Electron; Muramidase; Peutz-Jeghers Syndrome; Puromycin; Rats; Stomach Neoplasms; Stomach Ulcer; Triparanol; Whipple Disease; Zinc

Topics: Adolescent; Adult; Aged; Appendix; Atrophy; Autopsy; Biopsy; Chronic Disease; Female; Gastritis; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Humans; Ileum; Intestine, Small; Male; Metaplasia; Microscopy, Electron; Middle Aged; Muramidase

Topics: Duodenal Ulcer; Gastric Juice; Gastritis; Humans; Macromolecular Substances; Muramidase; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer