New spiral bacterium in gastric mucosa.

A new spiral bacterium, distinct from Campylobacter pylori, was found in the gastric mucosa of six patients with gastrointestinal symptoms. All patients had chronic active type B gastritis and four had oesophagitis. Culture and microscopy for C pylori infection was negative. These unculturable spiral organisms were probably an incidental finding in patients presenting for upper gastrointestinal endoscopy, but it is not possible to say from this small series whether these organisms cause chronic active gastritis. The organism is helical, 3.5-7.5 microns long and 0.9 micron in diameter with truncated ends flattened at the tips, and up to 12 sheathed flagella 28 nm in diameter at each pole. It is proposed that this spiral bacterium should be called "Gastrospirillum hominis Gen.nov., Sp.nov."     

Histopathological study of porcine gastric mucosa with and without a spiral bacterium ("Gastrospirillum suis").

Tightly spiralled bacteria ("Gastrospirillum suis") were seen in the pyloric mucosa of the stomach of 13 (10.8%) of 120 pigs that appeared clinically healthy at slaughter and in the fundic mucosa of three (5.0%) out of 60 pigs. The spiral organism could not be cultured from any pig. Chronic gastritis was observed in the pyloric mucosa of 53 (44.2%) of 120 pigs and in the fundic mucosa of 7 (11.7%) of 60 pigs. The 13 pigs with spiral bacteria in the pyloric region comprised one animal (7.7%) with normal pyloric mucosa, two (15.4%) with "borderline gastritis", and 10 (76.9%) with chronic gastritis--in one instance accompanied by signs of activity (numerous polymorphonuclear cells). The three pigs with spiral bacteria in the fundic mucosa comprised two animals with a normal fundic region and one with "borderline gastritis". The presence of the spiral bacterium was significantly associated with pyloric gastritis (p = 0.013) and with numbers of lymphoid follicles (p = 0.014).     

Prostaglandin E2 in gastric mucosa of children with Helicobacter pylori gastritis: relation to thickness of mucus gel layer.

AIMS--To evaluate the changes in mucus gel layer thickness and prostaglandin E2 (PGE2) content caused by Helicobacter pylori infection in the antral mucosa of children: to assess whether decreased mucus gel thickness is related to PGE2 production. METHODS--Antral biopsy specimens were taken at endoscopy from 153 children. H pylori gastritis was evident in 45 and normal mucosa in 59. The other 49 children were studied one month after antibiotic treatment that eradicated the infection in 37 of them had been stopped. One antral specimen was immersed in ice-cold saline, put under an inverse microscope with an eyepiece graticule. Mucus gel thickness was measured and then the processed for histological examination; another specimen was weighed and processed for in vitro prostanoid generation. RESULTS--Mucus gel layer thickness was significantly decreased in children with H pylori gastritis (90 (SD) 29) microns v 120 (58) microns in controls, p < 0.01) but returned to control values after H pylori had been eradicated. PGE2 generation was significantly increased in children with H pylori gastritis (1022 (811) ng/g v 641 (473) ng/g in controls, p < 0.01). One month after treatment PGE2 generation significantly decreased in children without infection (880 (534), p < 0.01), but was still high where infection persisted. A significant inverse correlation was found between PGE2 generation and mucus gel layer thickness (p < 0.05). CONCLUSIONS--These data suggest that H pylori damages the mucus gel layer, and that the gastric mucosa increases generation of PGE2 in response to back diffusion of acid and pepsin.     

Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children

We investigated the presence of Campylobacter pylori colonization of the gastric mucosa and of histologic evidence of gastritis in a prospective study of 71 consecutive children undergoing upper gastrointestinal tract endoscopy and gastric biopsies because of gastrointestinal symptoms. Two tissue samples from the gastric antrum were obtained from 67 of the 71 children (mean age [+/- SD], 11.4 +/- 3.8 years). One sample was evaluated for evidence of gastritis and stained with silver to detect organisms morphologically resembling campylobacter. The second sample was cultured for C. pylori, and a portion was used to perform a urease-screening test for the presence of C. pylori. Antral gastritis was diagnosed histologically in 18 of 67 patients. C. pylori was identified by both culture and silver staining on the antral mucosa in 7 of 10 patients with unexplained gastritis (primary gastritis) but in none of 8 patients with gastritis associated with an identifiable underlying cause (secondary gastritis). C. pylori was not identified in any of the 49 cases with normal histologic features. The urease-screening test was positive in only three of six patients with a positive culture for C. pylori. Duodenal ulcers were diagnosed by endoscopy in five patients. Each of the five had C. pylori on the antral mucosa, but organisms were not identified on the duodenal mucosa. We conclude that the presence of C. pylori on the antral mucosa is specifically associated with primary antral gastritis and may also be associated with primary duodenal ulceration.     

Immunocytochemical identification of Campylobacter pylori in gastritis and correlation with culture

Endoscopic biopsy specimens of antral mucosa from 25 patients presenting with gastric complaints were obtained for culture and histologic and immunocytochemical studies. The histopathologic study revealed chronic gastritis in 22 patients and borderline chronic gastritis in three patients. The unlabeled-antibody peroxidase-antiperoxidase (PAP) method was applied for the detection of Campylobacter pylori, and its results were compared with those obtained with the culture technique. Strongly positive immunoperoxidase staining was localized in spiral, curved bacteria that were present in the mucus layer adjacent to the gastric epithelial cell surface. The microorganisms were frequently congregated in clumps and were sectioned in several directions. The PAP stains were positive in 19 specimens (76%), and the cultures were positive in 20 (80%). All results negative by culture were also negative by PAP method. Compared with the cultures, the sensitivity and positive predictive value of the PAP method for identification of C pylori in antral mucosa obtained from endoscopic biopsy specimens were 95% and 100%, respectively.     

Intraepithelial infiltration by mast cells in human Helicobacter pylori active gastritis

Recent observations suggest an involvement of mast cells in Helicobacter pylori gastritis, but the mechanism of intraepithelial mast cell activation in H. pylori-infected patients remains to be clarified. Intraepithelial mast cells, identified by immunohistochemistry for CD117, were quantified in antral biopsies from 6 patients with H. pylori "active" chronic gastritis, 7 patients with H. pylori "nonactive" gastritis, and 9 controls. Antral biopsies from patients with H. pylori "active" gastritis showed higher intraepithelial mast cell counts than those from patients with H. pylori "nonactive" gastritis and from controls. Electron microscopy, selectively performed in 6 cases of H. pylori "active" gastritis, confirmed the presence of intraepithelial mast cells and allowed their subdivision into mature cells with intact electron-dense granules or degranulated cells. Other mast cells appeared to migrate through defects in the basement membrane into the epithelial layer. Mast cells in these areas often showed piecemeal degranulation or were characterized by large canaliculi, expanded Golgi areas, and a few granules, a process similar to the phase of recovery from anaphylactic degranulation of isolated human mast cells. The possible significance of these unusual ultrastructural findings is discussed.     

Experimental Helicobacter pylori gastric infection in miniature pigs

An experimental Helicobacter pylori infection in miniature pigs was developed and investigated. Eighteen miniature pigs were inoculated with an H. pylori strain that has high virulence in mice at c. 5 x 10(10) cfu. H. pylori infection in miniature pigs was achieved by the administration of agar 1% in brucella broth with fetal bovine serum 10% just before inoculation. The bacterial colonisation and distribution were analysed by mapping of viable cell counts in the stomach in pigs of three different ages. The mapping assay was achieved on post-infection day 3 for the 5-day-old and 2-week-old pigs, and between days 41 and 43 for 3-month-old pigs. The highest cell counts were observed in 5-day-old pigs, which averaged 4.9 x 10(6) cfu/g of mucosa (n = 4). The bacteria were colonised mainly in the cardiac and fundus gland region in the 5-day-old and 2-week-old pigs, whereas the colonisation sites did not depend on the region in the 3-month-old pigs. Biopsy assay of the antral mucosa of a 3-month-old pig after H. pylori infection showed that this infection persisted for >22 months. Serum antibody against H. pylori was detected in the infected pigs but not in the uninfected animal. Immunostaining demonstrated the presence of bacteria on the epithelial surface of the infected pigs. A microscopic finding common to all the infected pigs, focal gastritis with infiltration of lymphocytes detected on the lesser curvature of the stomach, resembled the microscopic appearance in H. pylori-infected human patients. These results suggest that miniature pigs might be a suitable model for studying H. pylori infection.     

Pathology of the gastric antrum and body associated with Helicobacter pylori infection in non-ulcerous patients: is the bacterium a promoter of intestinal metaplasia?

A series of 115 consecutive, non-ulcerous, dyspeptic patients were examined for Helicobacter pylori (H. pylori) colonization in the gastric antral and/or body mucosa using Giemsa staining. Findings were correlated with the presence and degree of activity of superficial gastritis, deep gastritis, atrophic gastritis and with the presence of intestinal metaplasia. The prevalence of H. pylori positivity was 61.7%. In 59 of the 71 positive patients (83%), H. pylori was detected in the antrum or in both the antral and oxyntic mucosa. In the remaining 12 positive patients, H. pylori was detected only in the oxyntic mucosa and in all these cases, the antrum showed intestinal metaplasia associated with atrophic gastritis (25%). In both antral and oxyntic mucosa, the activity of the gastritis was significantly correlated with H. pylori colonization. Linear logistic regression analysis showed that in patients with intestinal metaplasia the presence of H. pylori infection was significant in predicting the presence of more extensive intestinal metaplasia after adjusting for age. The prevalence of intestinal metaplasia types II and III was 65.5% in the H. pylori positive and 25% in the H. pylori negative patients. The antral mucosa is thought to be the elective site for H. pylori related histological lesions. At a later stage, H. pylori can be detected only in the oxyntic area while the antral mucosa shows extensive metaplastic or atrophic lesions. We would suggest that H. pylori plays a promotional role in the morphogenesis of intestinal metaplasia.     

Prevalence of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral and body mucosa.

AIMS--To evaluate the prevalence of lymphoid follicles and aggregates in the antral and body mucosa in Helicobacter pylori gastritis and to assess if there were correlations with ulcers in the duodenum, pylorus, or stomach, and with chronic antral erosions. METHODS--Patients (n = 2692) with histologically confirmed H pylori antral gastritis were investigated. These comprised five groups: those with duodenal ulcers; those with pyloric ulcers; those with gastric ulcers; those with chronic erosions; and those with no associated lesions. In 1446 cases at least two additional biopsy specimens from the oxyntic mucosa were available. RESULTS--Lymphoid follicles and aggregates were found in 53.8% of cases in the antral mucosa compared with 14.8% in the oxyntic mucosa (p < 0.001). The various diseases showed significant differences in terms of the prevalence of follicles and aggregates: The highest numbers in the antral mucosa as well as the lowest in the oxyntic mucosa were found in patients with duodenal ulcers (60.5% and 9.2%, respectively). The highest numbers of follicles and aggregates in the oxyntic mucosa occurred in patients with gastric ulcers. CONCLUSIONS--The detection of lymphoid follicles and aggregates in oxyntic mucosa and the higher prevalence in antral mucosa fits well with the distribution of primary gastric lymphomas. This adds further weight to the notion that the development of follicles and aggregates, triggered by H pylori, might be an early precursor to gastric lymphoma. The differences between the groups investigated might be due to different strains of H pylori or differences in the respective sizes of antral and oxyntic mucosa.     

An ultrastructural study of Helicobacter mustelae and evidence of a specific association with gastric mucosa.

The ultrastructure of Helicobacter mustelae, a natural inhabitant of the ferret stomach, has been studied and compared with the human gastroduodenal pathogen H. pylori. H. mustelae is a short, slightly curved rod, 2 microns x 0.5 micron, with four or more sheathed flagella. The most common flagellar configuration is a single flagellum at one terminus, bipolar arrangement at the other end and a lateral flagellum. Dense inclusion bodies were observed below the flagellar insertion sites. It is suggested that this configuration is a specialised adaptation to motility in a viscous environment. On examination of the ferret gastric mucosa, similarities to H. pylori were observed such as adherence to gastric tissue and the formation of adhesion pedestals. However, unlike H. pylori, significant numbers of bacteria were intracellular. Furthermore, a much greater proportion of H. mustelae were attached to the mucosa with few bacteria lying free in the mucus, as is seen with H. pylori. It is concluded that the ferret is an important model for the study of adherence of bacteria to gastric mucosa and their possible role in peptic ulceration.     

Identification of non-Helicobacter pylori spiral organisms in gastric samples from humans, dogs, and cats

Tightly coiled bacteria are a rare cause of gastric pathology in humans and represent a mixture of species for which a zoonotic origin is suspected. Similar organisms are common inhabitants of the gastric mucosae of carnivores and pigs. It was the goal of the present study to determine the actual occurrence of each individual Helicobacter species in human, canine, and feline stomachs in order to better understand the possible zoonotic significance. Gastric biopsy samples from humans with histological evidence of non-Helicobacter pylori spiral bacteria (n = 123) and samples from the gastric antrum, corpus, and cardia from dogs (n = 110) and cats (n = 43) were subjected to a multiplex PCR, enabling the identification of Helicobacter felis, Helicobacter bizzozeronii, Helicobacter salomonis, and "Candidatus Helicobacter suis." A PCR for detecting H. pylori was applied to all human samples. Single infections with "Candidatus Helicobacter suis," H. felis, H. bizzozeronii, H. salomonis, a hitherto unknown genotype of a non-H. pylori spiral organism (Helicobacter-like organism 135 [HLO135]), and H. pylori were identified in 30.9%, 8.9%, 2.4%, 11.4%, 7.3%, and 8.9% of the human biopsy samples, respectively. Mixed infections (16.3%) with two or even three of these were also found. In the canine stomach, H. bizzozeronii (70.0%) was encountered as the main spiral organism, while H. felis (62.7%) and HLO135 (67.4%) were the predominant Helicobacter species found in the feline gastric mucosa. Although the majority of human non-H. pylori organisms are Helicobacter species naturally occurring in the stomachs of pigs, cats, and dogs, the frequent identification of H. salomonis in human gastric biopsy samples is in contrast to its rare identification in pet carnivore samples, urging us to suspect other sources of infection.     

Detection of Helicobacter pylori DNA in the oral cavity and gastroduodenal system of a Venezuelan population

Dental plaque has been suggested as a reservoir for Helicobacter pylori but the hypothesis that the oral microflora may be a permanent reservoir of H. pylori is still controversial. The aims of this study were to determine the presence of H. pylori DNA in the gastric antrum and dental plaque of a Venezuelan population by PCR and to investigate the relationship between this infection and the oral hygiene index. Thirty-two patients from the Hospital Universitario de Caracas, attending for routine gastroscopy, and 20 asymptomatic subjects (control group) were evaluated. The patients' gingiva and plaque were assessed by the gingival and plaque indices of Sillness and L?e. Supragingival plaque was analysed by a PCR for a specific internal urease gene. Gastric antrum biopsies were taken for histological examination and PCR. H. pylori was detected in antral samples from 24 (75%) of 32 patients, all of whom had chronic gastritis. H. pylori was also detected in dental plaque samples of 12 (37.5%) of the 32 patients. In 7 (58%) of these 12 patients, H. pylori was identified in the gastric biopsy. Seven patients with chronic gastritis carried H. pylori in dental plaque and antral samples. Of these patients, four also had dysplasia and one had metaplasia. Three subjects in the control group were positive by PCR. In the present study there was no correlation between H. pylori infection and dental hygiene, dental caries, periodontal disease or use of dentures. The oral cavity may be a reservoir for H. pylori infection and oral secretions may be an important means of transmission of this micro-organism. H. pylori in dental plaque may represent a risk factor for gastrointestinal re-infection and ulcer relapse after antibiotic therapy.     

Campylobacter pylori is associated with chronic gastritis but not with active peptic ulcer disease

Campylobacter pylori is supposed to be involved in the pathogenesis of gastroduodenal peptic ulcer diseases and chronic gastritis. In order to study whether the Campylobacter pylori in the stomach of peptic ulcer patients is related to ulcer itself or to a co-existing chronic gastritis, we examined the frequency of the bacteria in Giemsa stained histological sections of biopsy specimens from a series of patients with active peptic ulcer and from series of non-ulcer control subjects. We found no difference in the frequency of Campylobacter- positive cases between ulcer patients and non-ulcer controls when the comparison was done within the same category of chronic gastritis; e.g., within the category of chronic superficial gastritis 74% and 78% of cases showed the bacteria in antral biopsies from ulcer patients and from non-ulcer controls, respectively. In both ulcer patients and control subjects, in similar way in both antral and body mucosa, the Campylobacter pylori was strongly associated with chronic superficial gastritis but was more weakly associated with chronic atrophic gastritis, and the bacteria were only occasionally seen in normal mucosa. We conclude that Campylobacter pylori is associated with chronic gastritis in peptic ulcer patients but is not related to active ulcer.     

Mast cells in Helicobacter pylori associated antral gastritis

Mast cells are known to be effector cells in various inflammatory reactions, but their role in gastritis is unclear. The present study was undertaken to investigate the extent of mast cell involvement in antral gastritis with and without Helicobacter pylori (H. pylori) infection and thus evaluate the possible role of mast cells in the pathogenesis of H. pylori-associated gastritis. Antral mucosal biopsies were taken from 212 subjects with symptoms suggestive of acid peptic disease. Sections were assessed for inflammation. Modified Giemsa stain was used to detect H. pylori infection and 1% toluidine blue to count mast cells. Mast cell counts were significantly higher in the antral mucosa even in H. pylori-negative gastritis (68.4 +/- 6.7/mm2), as compared to normal non-inflamed mucosa (45.7 +/- 5.8/mm2) (P < 0.05). However, with H. pylori infection, the mucosal mast cell count were markedly increased (123.8 +/- 4.7/mm2) as compared to normal mucosa (P < 0.01). and H. pylori-negative gastritis (P < 0.01) this increase was noticed uniformly in patients with H. pylori-positivity, irrespective of the presence or absence of a peptic ulcer. After cure of H. pylori infection, the mast cell density decreased significantly (44.9 +/- 4.6/mm2) to reach levels that were similar to those in normal mucosa. There was a positive correlation between the antral mucosal mast cell density and polymorphonuclear and mononuclear cell infiltration (rs = 0.61). H. pylori infection, and 0.73 respy. It was concluded that could be responsible for increasing the mast cell density in the gastric antrum. Probably by inducing castain mucosal cytokine.     

Helicobacter mustelae and Helicobacter pylori bind to common lipid receptors in vitro.

Helicobacter pylori is a recently recognized human pathogen causing chronic-active gastritis in association with duodenal ulcers and gastric cancer. Helicobacter mustelae is a closely related bacterium with similar biochemical and morphologic characteristics. H. mustelae infection of antral and fundic mucosa in adult ferrets causes chronic gastritis. An essential virulence property of both Helicobacter species is bacterial adhesion to mucosal surfaces. The aim of this study was to determine whether H. mustelae binds to the same lipids shown previously to be receptors for H. pylori adhesion in vitro. By using thin-layer chromatography overlay and a receptor-based enzyme-linked immunosorbent assay, H. mustelae was found to bind the same receptor lipids as H. pylori, namely, phosphatidylethanolamine and gangliotetraosylceramide. In addition, both H. pylori and H. mustelae bound to a deacylplasmalogen phosphatidylethanolamine. In contrast to H. pylori, H. mustelae binding to receptors was unaffected by motility or viability. Murine monoclonal and bovine polyclonal antibodies against exoenzyme S, and exoenzyme S itself (from Pseudomonas aeruginosa), inhibited binding of H. mustelae to phosphatidylethanolamine and gangliotetraosylceramide. These findings show that H. mustelae binds in vitro to the same lipid receptors as H. pylori and suggest that the adhesion of H. mustelae to such species is mediated by preformed, surface-exposed adhesins which include an exoenzyme S-like protein.     

Relation between IgG and IgA antibody titres against Helicobacter pylori in serum and severity of gastritis in asymptomatic subjects.

AIMS--To investigate whether the absorbance index of IgG and IgA antibodies against Helicobacter pylori is related to a semiquantitative assessment of the density of H pylori colonisation in gastric biopsy specimens and to the severity of gastritis. METHODS--The grade of gastritis was scored separately for antral and fundic mucosa using three different classifications. Serum IgA and IgG antibodies against H pylori were measured by ELISA. The density of gastric H pylori colonisation was graded semiquantitatively from 0 to 3. RESULTS--Among 48 healthy volunteers studied, 17 were found to have gastritis according to Whitehead''s criteria. H pylori was present in the biopsy specimens of 14 of 17 subjects with gastritis. The IgG H pylori antibody absorbance index was significantly (p < 0.05) correlated not only with the density of antral H pylori colonisation, but also with the degree of gastritis of the antrum, as assessed by the Whitehead score, activity, and the Sydney system (p < 0.05). The IgA H pylori antibody absorbance index was significantly correlated with the Whitehead score and Sydney system, but not with the activity score of the antrum or with the density of antral gastric H pylori infection. There were no significant correlations between the IgG H pylori antibody absorbance index and the gastritis scores of the fundus mucosa and the density of H pylori infection of the gastric body. The IgA H pylori antibody absorbance index was only significantly (p < 0.05) correlated with the density of H pylori colonisation and the Sydney system gastritis score of the corpus. CONCLUSIONS--The serological absorbance index of IgG antibodies against H pylori is related to the severity of antral gastritis and the density of antral H pylori colonisation. Thus a high absorbance index of IgG antibodies against H pylori points to severe antral gastritis and dense H pylori colonisation of the antrum.     

Omeprazole: its influence on gastric acid secretion, gastrin and ECL cells

The H+,K+-ATPase inhibitor omeprazole is a highly effective gastric antisecretory agent, both in animals and man, with a long duration of action. These properties are shared by a number of recently described histamine H2-receptor antagonists. In life-long oncogenicity studies of these H2-receptor antagonists, as well as with the H+,K+-ATPase inhibitor omeprazole, gastric enterochromaffin-like cell (ECL cell) hyperplasia and carcinoids have been found. The purpose of this paper is to summarize available evidence for the "Gastrin Hypothesis" to explain the development of ECL-cell hyperplasia. The hypothesis may be outlined as follows: 1) Inhibition of gastric acid secretion leads to elevated antral pH and, secondarily, to release of gastrin from the antral gastrin cells into the blood stream. 2) Gastrin causes both general hypertrophy of the oxyntic mucosa and hyperplasia of the ECL cells in the oxyntic mucosa. That this sequence of events occurs not only with omeprazole but also with other effective gastric antisecretory agents has been verified in the rat by giving the H2-receptor antagonist ranitidine as a continuous infusion. Ranitidine caused a hypergastrinemia of a similar magnitude as that seen after omeprazole, provided that the acid secretion was inhibited to a similar degree. At similar gastrin levels, ECL-cell hyperplasia of the same magnitude developed during both ranitidine and omeprazole treatment. Antrectomy prevented the development of ECL-cell hyperplasia during omeprazole treatment, indicating that the hyperplasia was not due to the drug treatment per se, but rather to the hypergastrinemia. Both the hypergastrinemia and the ECL-cell hyperplasia were found to be reversible.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ultrastructural study of Helicobacter pylori-associated gastritis

Endoscopic biopsies of antral mucosa from 26 patients with Helicobacter pylori-associated gastritis were studied by electron microscopy (EM). Scanning electron microscopy (SEM) showed clustering of H. pylori in the intercellular areas, being entrapped by the microvilli which were decreased at the sites where the bacilli were seen. The observations of SEM were confirmed by transmission electron microscopy (TEM), which showed adherence of the bacilli to the cell surface, producing cup-shaped depressions in the epithelial cells, and occasionally intracellular infiltration by H. pylori. There were also depletion of mucus granules, degenerative changes, and disruption of intercellular junction complexes of the epithelial cells. Post-treatment biopsies showed complete disappearance of the bacilli, and ultrastructural changes associated with H. pylori infection were resolved.     

Association of Helicobacter pylori with HLA-DR antigen expression in gastritis.

AIMS: To assess the association between Helicobacter pylori-associated gastritis and HLA-DR antigen (class II antigen) expression. METHODS: Fifty endoscopic gastric biopsy specimens were studied for the presence of H pylori, degree and type of inflammation, and for HLA-DR antigen expression in the epithelium. The cases were chosen to represent different categories: inflamed gastric mucosa with (n = 13) and without (n = 20) H pylori, and non-inflamed mucosa (n = 17). RESULTS: The antigen was aberrantly expressed in the antral mucosal epithelium in 11 of 12 cases (92%) with acute-on-chronic gastritis when H pylori was also present. It was present in the antrum in only seven of 18 H pylori negative cases (39%) with acute-on-chronic/chronic gastritis. One of three cases of acute gastritis and three of seven cases of chronic gastric erosions (non-inflamed category) showed positive staining. Generally, there was more staining in the antral than body mucosa and in the surface/foveolar epithelium than in the glands. No aberrant HLA-DR antigen expression was found in the 10 cases of normal gastric mucosa examined. CONCLUSIONS: These findings suggest that H pylori may have a role in the induction of class II HLA antigen expression in chronic gastritis and lend support to the view that these organisms may be responsible for part of the inflammatory response.