IgE-containing cells in gastric mucosa with and without Helicobacter pylori infection

Gastric mucosa responds with inflammation to Helicobacter pylori (H. pylori) infection. While numerous reports have shown that the immune system produces specific IgG, IgA, and IgM isotype anti H. pylori antibodies, IgE-mediated pathways of H. pylori-associated gastritis are mostly unknown. Our aim was to evaluate whether an increased presence of IgE in the antral gastric mucosa is responsible for the severity of the H. pylori-associated gastritis. The number of IgE-containing cells was estimated in formalin-fixed, paraffin-embedded antral gastric biopsy specimens using immunohistochemistry in three groups of patients: (i) 20 H. pylori-positive cases with moderate inflammation, (ii) 19 H. pylori-negative cases with moderate inflammation, and (iii) 19 H. pylori-negative cases with normal mucosa. In chronic gastritis, the number of IgE-positive cells increased significantly as compared to normal mucosa. In gastritic patients, H. pylori positivity was accompanied by a significant accumulation of IgE-positive cells, mainly plasma cells. These data suggest that IgE-mediated immune response probably plays an important role in the development of H. pylori-associated gastritis.     

Light and electron microscopic immunohistochemical investigation on G and D cells in antral mucosa in Helicobacter pylori-related gastritis.

Recently, it has been recognized that Helicobacter pylori (H. pylori) infection is associated with an exaggeration of basal and meal gastrin secretion. We investigate whether there is a relationship between H. pylori-related chronic gastritis and G-cell and D-cell number and granule density index of G and D cells. - The number of antral G cells and D cells and granule density index of D and G cells are compared between thirty two patients with H. pylori-related chronic gastritis and twelve patients without H. pylori and inflammation. Antral mucosal biopsy specimens are examined using light and electron immunohistochemical techniques. - The number of G cells is the same in either infected or uninfected patients (98.40 +/- 11.39, 109.25 +/- 12.76 vs 101.17 +/- 7.72 for infected patients with non atrophic and with mild atrophic chronic gastritis and uninfected controls, respectively) except for the cases with moderate gastric mucosal atrophy, where G cells (58.22 +/- 5.63) decrease in number. The number of D cells is decreased in all patients with H. pylori-related gastritis. G cell granule density index is significantly (p < 0.05) increased in patients with H. pylori-related chronic gastritis than in controls (3.15 +/- 0.43 vs 2.528 +/- 0.01). D cell granule density index is similar between patients with H. pylori chronic gastritis and controls (3.18 +/- 0.05 vs 3.166 +/- 0.12). It is concluded that decreased D cells number in patients with H. pylori-related chronic gastritis might be one of the reasons for the existing hypergastrinaemia.     

Involvement of mast cells in gastritis caused by Helicobacter pylori: a potential role in epithelial cell apoptosis

BACKGROUND: The role(s) of mast cells (MC) in gastric mucosal inflammation caused by Helicobacterpylori is (are) still debated. AIM: To determine whether there is an association between MC density and epithelial cell apoptosis in antral gastric mucosa infected by H pylori. Patients and methods: Biopsy specimens from 122 H pylori-positive subjects with chronic active gastritis, 84 patients with non-steroidal anti-inflammatory drug-induced gastritis and 48 volunteers were included. H pylori genotypes were determined by PCR amplification of bacterial cultures. Immunohistochemical analysis was performed on tissue microarrays with anti-CD117, anti-chymase, anti-tryptase, anti-myeloperoxidase, anti-Bcl-2, anti-Bcl-x, anti-Bax and anti-caspase 3 antibodies. RESULTS: Of the 122 patients infected with H pylori, 76 (62.3%) harboured cagA positive strains. H pylori isolates belonged to the vacAs1/m1 genotype in 82 (67%) cases, to the vacAs2/m2 genotype in 23 (18.8%) cases and to the vacAs1/m2 genotype in 17 (13.9%) cases. 61 (50%) H pylori isolates were babA2+. In patients infected with H pylori, the density of MC, and in particular the number of MC-associated epithelial cells, was correlated with a high number of apoptotic epithelial cells. Moreover, the density of MC was correlated with the number of neutrophils infiltrating the antral gastric mucosa, and was strongly increased in patients infected with cagA, vacAs1/m1 and babA2 positive strains. CONCLUSIONS: Taken together, these data show that the density of MC can be considered as a histopathological criterion of gastritis activity in patients infected with H pylori.     

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

BACKGROUND: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. AIM: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints. METHODS: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa. RESULTS: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased. CONCLUSIONS: Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.     

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.     

Impact of Helicobacter pylori eradication on morphological changes in gastric mucosa

The purpose of the study was to examine gastric mucosal morphological changes in patients with gastroduodenal pathology after eradication therapy for Helicobacter pylori (H. pylori). A hundred and thirty-eight patients (40 females and 98 males) were examined. Of them, there were 122 patients with duodenal peptic ulcer, 8 with gastric peptic ulcer, 5 with erosive gastritis, 2 with chronic atrophic antral gastritis, and 1 with non-atrophic gastritis. Two months and a year after therapy, manifestations of gastric mucosal atrophy, the degree of inflammation, and its activity significantly diminished in patients with complete H. pylori eradication. Positive changes were observed mainly in the antral portion of the stomach. In patients with partial eradication, chronic inflammation and its activity became less. Two months and a year following therapy, positive changes in the gastric mucosa were absent in patients without H. pylori eradication.     

Gastric Interleukin-8 and IgA IL-8 Autoantibodies in Helicobacter pylori Infection

Gastric infection with Helicobacter pylori is frequently characterized by neutrophil infiltration. The production of the neutrophil-activating peptide (NAP-1/IL-8) and mucosal IgA autoantibodies to IL-8 by human antral biopsies have been examined during short-term in vitro culture. Detectable IL-8 was secreted by 84% of H. pylori- negative patients with normal antral mucosa (range <0.07–61.5 ng/mg biopsy protein, n =19). Concentrations in 4 patients with reactive gastritis and 10 with inactive gastritis were not significantly different from subjects with normal mucosa. In H. pylori- positive patients with active gastritis and neutrophil infiltration into the epithelium ( n =17) IL-8 secretion was significantly increased relative to subjects with normal mucosa ( p > 0.0001), inactive gastritis ( p <0.001) and reactive gastritis ( P <0.01). IL-8 concentrations in active gastritis were significantly correlated with the extent of epithelial surface degeneration ( r =0.64). IgA autoantibodies were present in 19 patients (13 active, 4 inactive gastritis) and concentrations were significantly correlated with IL-8 production ( p <0.001). Gastric synthesis of IL-8 is likely to be an important factor in regulating mucosal neutrophil infiltration and activation in patients with H. pylori infection. The local production of IgA antibodies to IL-8 may represent a down-regulatory response of the host to limit mucosal damage associated with a chronic bacterial infection.     

Effect of Helicobacter pylori infection on epidermal growth factor receptor (EGFR) expression and cell proliferation of gastric epithelial mucosa: correlation to macroscopic and microscopic diagnosis

Our aim was to compare the expression of EGFR and proliferative cell nuclear antigen (PCNA) in different histological and endoscopic diagnostic groups, in cases of Helicobacter pylori infection, in vivo. Paraffin embedded human gastric biopsy samples (86) were analysed by EGFR and PCNA immunohistochemistry and classified both on the basis of histology and endoscopic findings. In normal epithelia (NE), a positive correlation was found between PCNA and EGFR and in H. pylori-negative gastritis with and without intestinal metaplasia (P < 0.01). On the other hand, a negative correlation was detected between the two immunohistochemical findings in H. pylori-associated gastritis with intestinal metaplasia (HPGIM) and in the atrophic gastritis (AG) group. In HPGIM the percentage of EGFR-positive cells was significantly lower (32.4 +/- 30.4) when compared to either the NE (50.3 +/- 23.7) or H. pylori-negative gastritis with intestinal metaplasia (HNGIM) (48.3 +/- 23.7). In AG, EGFR was significantly lower when compared to the NE (P < 0.05). Based on the endoscopic findings, a significant decrease of EGFR expression was found in gastric ulcer cases as compared to NE, gastritis or erosion cases (P < 0.01). PCNA showed no significant alterations between the NE and gastritis, AG groups. The presence of H. pylori has an inverse effect on PCNA and EGFR expression in HPGIM.     

Helicobacter pylori gastritis in cats with long-term natural infection as a model of human disease

A natural infection with Helicobacter pylori (H. pylori) in domestic cats (Felis cattus) less than 2 years of age has been well described in a closed colony of animals. Six cats from this colony that were serially evaluated by culture, polymerase chain reaction, and light and electron microscopy for a period of 3 years demonstrated persistent gastric colonization with a single cag(-) vac(+) strain of H. pylori. In these cats, as well as five other 5- to 6-year-old cats that were examined, a long-term infection resulted in chronic diffuse lymphofollicular atrophic gastritis with areas of mucosal dysplasia in the antrum and predominantly midsuperficial gastritis in the body and cardia. Topographically, the distribution of lesions was similar in both young and older cats and closely resembled that found in humans, with the most severe changes occurring in the gastric antrum. Few granulocytes and no significant elevation in mast cells were seen in older H. pylori-infected cats compared with uninfected controls; however, marked increases in interepithelial globule leukocytes and numerous active mucosal lymphoid follicles were present in infected animals. Indices of gastritis were significantly greater in older infected cats when compared with uninfected controls and younger cats (P < 0.05). The antral cell proliferation index of infected older cats was significantly (P = 0.021) greater than that of uninfected controls. Apoptotic indices of the gastric antrum and body of infected cats were significantly (P = 0.01) increased versus controls. Chronic infection with H. pylori in cats shares many features of long-term H. pylori infection in humans, including the development of preneoplastic processes. This similarity provides useful, comparative insights into host-pathogen interactions.     

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.     

Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection.

Childhood acquisition of Helicobacter pylori is a critical risk factor for gastric cancer. Since tumorigenesis involves deregulation of proliferation and apoptosis, we examined gastric epithelial cell proliferation and apoptosis in H. pylori-infected children. Apoptosis and proliferation of gastric antral epithelial cells in biopsy specimens from patients with H. pylori-induced gastritis, secondary gastritis, and noninflamed controls were compared. p53 protein expression was examined immunohistochemically. Apoptotic cells were identified in the surface epithelium in each group. The apoptotic index was higher in specimens from patients with H. pylori gastritis (120 +/- 10) than secondary gastritis (50 +/- 10) and noninflamed controls (40 +/- 10, analysis of variance P < 0.005). Apoptosis decreased following H. pylori eradication and resolution of gastritis (P < 0.02). An expanded proliferative compartment was identified in H. pylori-induced gastritis (32.4 +/- 3.5; proliferative labeling index +/- SE) compared with secondary gastritis (18.9 +/- 2.8) and noninflamed controls (13.7 +/- 3.1, analysis of variance P < 0.01). The accelerated cell turnover was associated with p53 overexpression (analysis of variance P < 0.005). Accumulation of p53 was not associated with expression of the cyclin-dependent kinase inhibitor p21. The occurrence of altered cell turnover early in the natural history of chronic infection provides an explanation for the increased risk of gastric cancer development associated with childhood acquisition of infection.     

Argyrophilic nucleolar organizer regions in Helicobacter pylori-associated gastric lesions

Three hundred and fifty biopsies from patients undergoing upper gastrointestinal endoscopy were studied for histopathological changes, H. pylori infection and argyrophilic nucleolar organizer region (AgNOR) counts. Histopathological examination revealed normal gastric mucosa in 10 (2.85%), gastritis in 254 (72.56%), intestinal metaplasia in 12 (4.0%), dysplasia in 13 (3.7%) and adenocarcinoma in 61 (17.4%). The mean (SD) AgNOR count was 1.66 (0.20) in normal, 2.43 (0.64) in gastritis, 3.09 (0.52) in intestinal metaplasia, 4.17 (0.31) in dysplasia, and 6.57 (0.98) in carcinoma. A statistically significant difference was observed between the AgNOR count of normal gastric mucosa and gastritis (p<0.001), gastritis and dysplasia (p<0.001), and dysplasia and adenocarcinoma (p<0.001). A statistically significant increase in mean AgNOR count was found with increase in H. pylori density in gastric biopsies (p<0.001) with gastritis. No significant difference was observed between mean AgNOR count of intestinal and diffuse type carcinomas. The AgNOR count in gastric biopsies with adenocarcinoma and H. pylori infection was 7.03 (0.85) as compared to 6.89 (0.73) in gastric biopsies with evidence of adenocarcinoma but without H. pylori infection. The difference was not statistically significant. The findings support the role of H. pylori as a promoting agent in gastric carcinogenesis by stimulating gastric epithelial cell proliferation at the stage of chronic inflammation, thereby making the cells more susceptible to endogenous or exogenous carcinogenic agents.     

Helicobacter pylori associated gastric diseases and lymphoid tissue hyperplasia in gastric antral mucosa

AIM: To investigate the relation between Helicobacter pylori associated gastroduodenal diseases and lymphoid tissue hyperplasia in the antral mucosa and to pursue its evolution after eradication of H pylori. METHODS: Gastric antral biopsy specimens were obtained from 438 patients with H pylori positive gastroduodenal diseases (185 chronic gastritis, 69 gastric ulcer, and 184 duodenal ulcer) and 50 H pylori negative healthy controls. Lymphoid follicles and aggregates were counted and other pathological features were scored according to the updated Sydney system for classification of chronic gastritis. After a course of anti-H pylori treatment, biopsy specimens were obtained at four to six weeks, 12 months, and 24 months in the chronic gastritis patient group. RESULTS: The total prevalence of lymphoid follicles and aggregates in the biopsies was 79.9% (350 of 438; 95% confidence intervals (CI), 0.76 to 0.84). The prevalence and density of lymphoid follicles and aggregates were significantly different in the various gastroduodenal diseases. The highest prevalence (89.9%; 95% CI, 0.83 to 0.97) and density (0.82) of lymphoid follicles and aggregates occurred in patients with gastric ulcers. The lowest prevalence of lymphoid follicles and aggregates was found in patients with chronic gastritis (74.6%; 95% CI, 0.68 to 0.81), and the lowest density of lymphoid follicles and aggregates (0.56) was seen in patients with duodenal ulcers. The prevalence and density of lymphoid follicles and aggregates correlated strongly with the activity and severity of gastric antral mucosal inflammation. The eradication of H pylori resulted in a decrease in the prevalence and density of lymphoid follicles and aggregates. CONCLUSION: The prevalence and density of lymphoid follicles and aggregates in gastric antral mucosal biopsies correlated closely with H pylori infection.     

The immunoexpression of Tn, sialyl-Tn and T antigens in chronic active gastritis in relation to Helicobacter pylori infection

The simple mucin-type carbohydrate antigens Tn, sialyl-Tn and T represent the mucin core oligosaccharide structures that are produced in the initial steps of mucin biosynthetic pathway. Utilising monoclonal antibodies anti-Tn antigen, anti-sialyl-Tn antigen and anti-T antigen, we have investigated the expression of the simple mucin-type carbohydrate antigens in 47 biopsy specimens of antral mucosa with chronic active gastritis, 25 of which had Helicobacter pylori infection. The Tn immunoreactivity, localised at the supranuclear region of surface and glandular mucous cells, was observed in all samples, independently from H. pylori status. The sialyl-Tn antigen, mainly localised in the cytoplasm of glandular mucous cells and in goblet cells vacuoles, was seen in 56% of the cases with H. pylori infection and in 41% of the cases in the H. pylori-negative group. In addition, the T antigen was found in the cytoplasm of surface and glandular mucous cells in 16% of the H. pylori-positive group, whereas the percentage of positive cases was reduced to 5% in H. pylori-negative patients, with an exclusive localisation in the cytoplasm of glandular mucous cells; after neuraminidase treatment, the percentage of T antigen-positive cases was increased to 28% in H. pylori-positive cases and to 27% in negative cases. No significant relationships between H. pylori infection and Tn, sialyl-Tn or T antigen immunoexpression were encountered in our cases. Therefore, we maintain that the inflammatory infiltrate may itself play an important role in the expression of simple mucin-type carbohydrate antigens in chronic active antral gastritis.     

Relationship of CagA to serum gastrin concentrations and antral G, D cell densities in Helicobacter pylori infection.

The purpose of this study was to investigate whether the densities of antral gastrin and somatostatin-immunoreactive cells in Helicobacter pylori (H. pylori) infection were related to the bacterial expression of cytotoxin-associated gene A (CagA). 32 patients who had underwent diagnostic esophagogastroduodenoscopy were studied. On the histologic examination all patients had antral gastritis. We divided the subjects into three groups. Group I consisted of 6 patients who had chronic superficial gastritis, group II, 9 patients who had H. pylori-associated gastritis but with no expression of CagA, and group III, 17 patients who had H. pylori-associated gastritis with the expression of CagA. In group I and II, serum gastrin levels, and antral G cell and D-cell were measured. In group III, serum gastrin levels, and antral G cell and D-cell were measured, before and after the eradication of H. pylori. The results were as follows. Firstly, serum gastrin concentrations were significantly higher in the patients with H. pylori infection than in the negative controls. Nextly, there was no correlation between the changes in antral G or D-cell density and H. pylori infection. Thirdly, group III had a significant increase in serum gastrin concentrations and a significant decrease in antral D-cell density than group I. Forthly, eradication of H. pylori in group III showed a significantly increased antral D-cell density. Our results suggest that hypergastrinemia in H. pylori-associated gastritis is relevant to the presence of CagA, and the possible mechanism of hypergastrinemia may be related to antral D-cell deficiency, which is caused by H. pylori infection with the expression of CagA.     

Immunoglobulin G antibody against Helicobacter pylori: clinical implications of levels found in serum

The clinical significance of high levels of antibody against Helicobacter pylori is still unclear. We sought to evaluate whether the serum antibody levels could predict the presence of macroscopic gastroduodenal disease, to identify factors that correlate with antibody levels in a multivariate context, and to determine the predictive value of antibody levels for diagnosing H. pylori infection. The grades of gastritis and density of H. pylori colonization were scored separately using the updated Sydney system for antral and body mucosa. An enzyme-linked immunosorbent assay (ELISA) for the quantitative detection in serum of IgG antibodies to H. pylori was performed. Of the 170 dyspeptic patients, 105 (62%) had H. pylori infection. There was no difference in antibody levels among endoscopic findings of normal mucosa, chronic gastritis, and duodenal ulcer. On multivariate linear regression analysis, the status of H. pylori infection, mononuclear cell infiltration of body mucosa, and age correlated with antibody levels. The negative predictive value for antibody levels of <30 U/ml is 94%, and the positive predictive value of antibody levels of >70 U/ml is 98%. We conclude that serum antibody levels do not predict the severity of gastroduodenal diseases or the density of H. pylori colonization in H. pylori-infected dyspeptic patients. Higher levels are associated with the presence of H. pylori infection, the chronic gastritis score of the corpus, and older age. Setting a gray zone is necessary for ELISA, since the accuracy in this zone does not allow a precise determination of H. pylori status.     

Helicobacter pylori-induced gastritis in the domestic cat.

Helicobacter pylori has been cultured from the inflamed gastric mucosae of naturally infected cats; the lesions in H. pylori-infected cat stomachs mimic many of the features seen in H. pylori-infected human stomachs. To determine whether H. pylori-negative specific-pathogen-free cats with normal gastric mucosae were susceptible to colonization by this bacterium and whether gastritis developed after infections, four H. pylori-negative cats treated with cimetidine were orally dosed three times with 3 ml (1.5 x 10(8) CFU/ml) of H. pylori every 4 days. All four cats became persistently colonized as determined by gastric cultures and PCRs from serial gastric biopsy samples and necropsy samples at 7 months postinfection. H. pylori was not isolated from the two control cats, nor were their gastric tissues positive by PCR; one of the two cats had a few focal lymphocytic aggregates in the body submucosa, whereas the second cat had a normal gastric mucosa. All four H. pylori-infected cats had multifocal gastritis consisting of lymphoid aggregates plus multiple large lymphoid nodules, which were most noticeable in the antral mucosa. In addition, one H. pylori-infected cat had a moderate diffuse infiltration of polymorphonuclear leukocytes in the subglandular region of the antrum. H. pylori-like organisms were focally distributed in glandular crypts of the antrum. Two of the H. pylori-infected cats had significant (eightfold) increases over baseline in levels of immunoglobulin G H. pylori serum antibody. The H. pylori isolates from the four experimentally infected cats had restriction fragment length polymorphism patterns specific for the flaA gene that were identical to those of the inoculating strain. H. pylori readily colonizes the cat stomach and produces persistent gastritis.     

Serum CagA antibodies in asymptomatic subjects and patients with peptic ulcer: lack of correlation of IgG antibody in patients with peptic ulcer or asymptomatic Helicobacter pylori gastritis.

AIM/BACKGROUND: Several studies have suggested that Helicobacter pylori which express CagA may be more virulent than those that do not, but limited populations have been studied to date. The aim of this study was to confirm and extend the association of CagA positive H pylori strains in a different geographical area and to a large, well defined patient population. METHOD: A validated ELISA for serum IgG to CagA was used to investigate the prevalence of CagA seropositivity in 100 patients with peptic ulcer compared with 77 with H pylori infection without ulcer disease in a North American population. The extent of antral and corpus inflammation and H pylori density in relation to CagA seropositivity in 40 subjects with H pylori infection were assessed semiquanitatively. All studies were carried out in a coded and blinded manner. RESULTS: The prevalence of serum IgG CagA antibodies was higher in H pylori infected patients with ulcer (59%) compared with healthy H pylori infected volunteers (44%), but the difference was not significant. In contrast, the titre of serum IgG anti-CagA antibodies was higher among the seropositive subjects without ulcer disease, but again the difference was not significant. Comparison of histological features between asymptomatic individuals with H pylori infection in relation to CagA IgG antibody status revealed no differences in infiltration with acute inflammatory cells, H pylori density, or gastritis index. There was no relation evident between the degree of polymorphonuclear cell infiltration and the serum IgG antibody titre to CagA. Mononuclear cell infiltration in the antrum, but not the corpus, was greater in those with CagA IgG compared with those without (median score 5 v 3). CONCLUSIONS: A right association between the presence or titre of serum IgG to CagA and peptic ulcer disease, greater H pylori density or infiltration of the mucosa with acute inflammatory cells could not confirmed in a North American population. Perhaps geographical differences in the prevalence of circulating H pylori strains are responsible for the discrepant results reported.