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Background: Interleukin-1 receptor antagonist genotype 2/2 is associated with a prolonged and enhanced inflammatory response. It is suspected of being a risk factor for atrophic gastritis and gastric cancer and for some autoimmune diseases. No specific genetic risk factors for oesophagitis have been identified so far and there are no reports of IL-1 polymorphism in relation to oesophageal disease., Methods: We studied the IL-1RN, IL-1beta-511 and IL-1beta + 3953 polymorphisms in an unselected series of 142 adult patients scheduled for gastrointestinal endoscopy because of dyspepsia. The control group consisted of university staff and students (n = 179). Helicobacter pylori status was determined by antibody testing and bacterial detection., Results: Endoscopic oesophagitis was noted in 40 patients. The IL-1RN 2/2 genotype was significantly more prevalent in the patients with H. pylori-negative oesophagitis than in the control subjects (27% versus 9%; OR 3.574, CI 1.23-10.35, P = 0.034) or in the dyspeptic patients (27% versus 7%; OR 5.089. CI 1.51-17.11, P = 0.009). IL-1beta-511 T/T genotype tended to be more frequent in the H. pylori-negative patients with oesophagitis than in the control subjects (P = 0.071). The strongest association was between the simultaneous carriage of genotypes IL-1RN 2/2 and IL-1beta -511 T/T and H. pylori-negative oesophagitis. where the combined genotype was more prevalent than in the control subjects (23% versus 6%; OR 4.492, CI 1.40-14.46, P = 0.012) or the dyspeptic patients without oesophagitis (23% versus 3%: OR 9.706. CI 2.12-44.42, P = 0.003)., Conclusions: The results indicate that the IL-1RN 2/2 genotype and the carriage of combined genotypes IL-1RN 2/2 + IL-1beta-511 T/T are associated with H. pylori-negative oesophagitis. This is the first report on the association between IL-1 gene polymorphism and oesophagitis.

The etiology of chronic gastric erosions is unknown. We have evaluated the significance of Helicobacter pylori and herpes simplex virus (HSV) infections, the use of nonsteroidal antiinflammatory drugs (NSAIDs), alcohol, and smoking in a prospective long term follow-up study. A prospective series of 117 patients with gastric erosions and 117 controls were studied in 1974-1981, and invited for reendoscopy in 1996. At both visits, H. pylori infection was diagnosed by histology, serum HSV antibodies were measured, and the use of NSAIDs, alcohol, and smoking was evaluated by interview. Biopsies from erosions from the latter visit were studied for HSV by immunohistochemistry and polymerase chain reaction (PCR). In the follow-up visit, 16 of 42 patients had still gastric erosions while six of 47 controls had developed erosions. No HSV antigen or DNA could be detected in biopsy specimens. However, only high antibody titers (> or = 32) against HSV at the first visit predicted persistence of erosions (P = 0.000), while H. pylori infection, use of NSAIDs, alcohol, or smoking were not associated with chronic erosions. High HSV titers at the follow-up visit were also significantly associated with concurrent erosions in the patient group. In conclusion, the results suggest that a significant proportion of chronic gastric erosions are related to HSV infection.

Background: The mechanisms for the observed low prevalence of Helicobacter pylori infection in inflammatory bowel disease (IBD) are unknown, but might be important for the pathogenesis of IBD. We have studied the seroprevalence of H. pylori in different categories of IBD and evaluated the role of medical therapy, smoking and social status. We also analysed the effect of seropositivity on the age of onset of IBD in order to find possible evidence for the protective effect of the infection., Methods: We studied 296 (mean age 43 years, range 18-79; women 144) unselected patients with IBD, including 185 with ulcerative colitis (UC). 94 with Crohn disease (CD), and 17 with indeterminate colitis (IC). Seventy healthy age- and sex-matched subjects served as controls. Serum samples were studied for H. pylori antibodies. Detailed clinical history was obtained from patient records and by face-to-face interview., Results: The prevalence of H. pylori infection was lower in IBD patients (24%) than in controls (37%; P = 0.029), and in CD lower (13%) than in UC (30%; P = 0.002). Seropositivity was not related to sulphasalazine treatment or smoking. Age of onset of IBD was higher in seropositive (mean 40 years) than in seronegative patients (30 years: P < 0.001). The age of onset of IBD showed unimodal distribution in H. pylori seronegative patients, with a peak between 30 and 40 years, although there was some evidence of bimodality in CD. In contrast, H. pylori seropositive patients had clear bimodal pattern with peaks at 20-40 and 50-60 years of age., Conclusions: Our results confirm the low prevalence of H. pylori infection in IBD, and in particular in CD. The significantly higher age of onset and bimodal pattern of age-specific incidence in seropositive IBD patients suggest that H. pylori infection significantly modifies the development of IBD and may have a protective effect.

Background/aims: Lymphocytic gastritis is a subtype of chronic gastritis characterized by a marked increase in the number of intraepithelial lymphocytes in the gastric mucosa. Its etiology is unknown, but a proportion of these patients have Helicobacter pylori infection. The aim was to assess the significance of H. pylori treatment in lymphocytic gastritis patients., Methodology: The 10 patients with lymphocytic gastritis and either serologically or histologically diagnosed H. pylori infection were treated with a triple therapy and followed by serology and histology after 6-18 months., Results: The levels of IgG antibodies for H. pylori decreased below 50% of the pretreatment values in all patients. The maximum numbers of intraepithelial lymphocytes decreased significantly (P = 0.005) from the pretreatment values., Conclusions: Treatment of H. pylori infection cures lymphocytic gastritis associated with H. pylori infection. H. pylori appears to be one etiological cause of lymphocytic gastritis.

Helicobacter pylori induces signaling cascades leading to changes in cytoskeleton and an inflammatory response. Information on the morphological changes and cytoskeletal rearrangements induced by attachment of the bacterium is contradictory and signal transduction pathways are not well known. Since rho family of small GTPases is known to mediate cytoskeletal response to various extracellular stimuli, and is also involved in several other important signal transduction pathways, we have investigated the role of rac and cdc42 in H. pylori-induced cytoskeletal changes in cultured carcinoma AGS cells. AGS cells grown with serum expressed actin filaments in the form of short stress fibers and thin network at the edges, which were depolymerized by removal of serum. In serum-starved cells both type I and type II strains of H. pylori induced formation of actin filaments and lamellipodia-like structures. Microinjection of active rac induced similar changes, but injection of inactive rac prevented the effects of H. pylori, while active or inactive cdc42 did not have any significant effect. Cytoskeletal effects of H. pylori were inhibited by actinomycin D, but not completely by cycloheximide. These results indicate that rac activation is involved in signal transduction cascade leading to cytoskeletal reorganization induced by H. pylori and that gene activation and synthesis of new proteins is necessary in this process., (Copyright 2000 Academic Press.)

Background: We studied the mRNA expressions of interferon-gamma (IFN-gamma), interleukin-10 (IL-10), and IL-12 in gastric biopsy and blood samples from patients with and without Helicobacter pylori infection, by reverse-transcription polymerase chain reaction (RT-PCR)., Methods: RT-PCR was performed on total RNA preparations, and the expressed mRNA were semiquantitated on the basis of band intensities on Southern blots., Results: In gastric mucosa the expression of IFN-gamma and IL-10 was found in most patients with and without H. pylori infection, whereas IL-12 was found in most of the infected ones. The level of IFN-gamma and IL-10 did not differ between groups, whereas the IL-12 level was significantly higher in those with H. pylori infection. In the blood IFN-gamma expression was found in most samples, with higher level in patients with gastritis than in normals. Few blood samples (33%) had IL-12, and none had IL-10., Conclusion: IFN-gamma and IL-10 expressions in healthy mucosa may indicate a biologic role in a healthy state. IL-12 expression in mucosa was related to the presence of bacterial stimulant and therefore resembles proinflammatory cytokines.

Helicobacter pylori is the causative agent of chronic gastritis, peptic ulcers, and is also associated with gastric cancer. Eradication of H pylori infection has proven to be difficult to confirm. The authors developed a nonradioactive in situ hybridization method for detection of H pylori and compared it with conventional methods for diagnosis of the infection. Reverse transcription followed by polymerase chain reaction (PCR) with two 22-base primers was used to amplify a 520 base pair (bp) segment of 16S rRNA from H pylori. The PCR product was labeled with digoxigenin and used as a probe. Specificity of the probe was tested by dot blot hybridization against DNA from 30 different strains of related and unrelated bacteria. Specificity of in situ hybridization assay was proven by the lack of hybridization on sections with gram negative and positive bacteria other than H pylori, with an unrelated probe, without probe, and after RNase treatment. A random sample of 15 biopsy specimens was blindly studied by in situ hybridization method and the results were compared with those of culture and conventional histology. Comparison of in situ hybridization and conventional histology showed agreement in all 15 specimens (5 negative and 10 positive). Between culture and in situ hybridization there was agreement in 13 cases (8 positive, 5 negative). Two cases were negative by culture but positive by in situ hybridization and histology. Nonradioactive in situ hybridization provides a sensitive and specific method for detection of H pylori infection. It should be particularly useful for confirmation of infection in cases equivocal with other methods, and potentially useful in post-treatment evaluation.

Helicobacter pylori causes a chronic infection in gastric mucosa, but its systemic effects are largely unknown. Our aim was to characterize the effect of H. pylori infection and gastric mucosal inflammation on the peripheral blood leukocyte count. An endoscopic series of 96 patients (40 men and 56 women), with a mean age of 62 years (range 49-80) was studied. Endoscopy with eight stepwise biopsies was performed and the occurrence of H. pylori was studied from sections stained with Warthin-Starry. The severity of inflammation in antral and body mucosa was estimated. The peripheral blood leukocyte count and differential count were determined by the automatic flow cytometric method. The total number of blood leukocytes and the numbers of lymphocytes and basophils were significantly increased in H. pylori-positive patients (N = 58), as compared with H. pylori-negative ones (N = 38). The total number of blood leukocytes correlated with the numbers of neutrophils, eosinophils, and mononuclear cells in the gastric mucosa. The number of basophils correlated with the number of mucosal neutrophils and mononuclear inflammatory cells. The results show that mucosal inflammation due to H. pylori infection is reflected in the amount of peripheral blood leukocytes. Basophilia suggests involvement of allergic mechanisms in H. pylori gastritis.

Objective: To investigate the relation between Helicobacter pylori infection and coronary heart disease (CHD)., Design: A case-control study., Setting: Northern Finland (about 650,000 inhabitants)., Patients: 116 patients with angiographically documented CHD and 116 controls matched for age and gender randomly recruited from the register of the Finnish Social Insurance Institute., Main Outcome Measures: The odds ratio (OR) estimates for the association of H pylori infection with CHD., Results: 64% of the CHD patients and 53% of the controls were seropositive for H pylori; the OR adjusted for age and gender was 1.5 (95% confidence interval (CI) 0.9 to 2.5). An additional adjustment for the common risk factors of CHD, including lipid concentrations, in a logistic regression analysis produced an OR estimate of 1.1 (95% CI 0.6 to 2.1). Among the controls, those who were H pylori positive had significantly (P = 0.03) higher concentrations of serum triglycerides than those who were H pylori negative: the trend among the cases was similar, but non-significant. The concentrations of HDL cholesterol tended to be lower in those who were H pylori positive than in those who were H pylori negative, among both the cases and the controls., Conclusions: The impact of H pylori infection as an independent risk factor for CHD seems to be minor. On the other hand the results are consistent with the hypothesis that H pylori infection might modify the serum lipid concentrations in a way that could increase the risk of CHD.

The histopathologic detection of Helicobacter pylori in gastric biopsy specimens is considered the gold standard for the diagnosis of H pylori infection. However, few studies have addressed the pathologists' reliability to detect the organism and to assess the degree of the related inflammatory changes. The objectives of this study were to determine the degree of agreement among the findings of four gastrointestinal pathologists in the semiquantitative evaluation of H pylori infection and gastritis. Three slides from specified areas of the stomach of 99 patients with and without H pylori infection were stained with the triple stain, coded, and examined independently by four pathologists. For each specimen, a visual analogue scale graded from 0 (absent/normal) to 5 (maximal intensity) was used to score (1) H pylori (2) neutrophils, and (3) atrophy. Data were analyzed using kappa-statistics. The kappa-coefficient for the detection of H pylori (present vs absent) was approximately .9 (excellent); for the intensity of infection, it was considerably lower on the 6-point scale (approximately .61) and improved slightly on an amalgamated 4-point scale (approximately .71). The agreement on presence or absence of neutrophils was excellent (kappa = .8) in antral biopsies and good (kappa = .67) in corpus biopsies. The kappa for the semiquantitative scoring of neutrophils was poor on the 6-point scale (approximately .43) and fair on the amalgamated scale (approximately .54). The interobserver agreement was the poorest in the evaluation of atrophy (presence, absence, categories, or group categories) with kappa coefficients varying from .08 and .29. This group of pathologists had a high level of concordance on the diagnosis of H pylori infection in any particular patient and a high index in the assessment of the intensity of infection. The agreement was less in the semiquantitative evaluation of active inflammation. When the evaluation concerned a loosely defined feature, such as atrophy, there was essentially no agreement among the pathologists. This study suggests the need for further assessments of pathologists' ability to provide reproducible diagnoses. These results also indicate that more stringent criteria for the diagnosis of "soft" histopathologic features (such as atrophy) are urgently needed.

Aims: To examine the course of lymphocytic gastritis and its relation to Helicobacter pylori (H pylori) infection in a 10 year follow up., Methods: Ninety six patients were originally examined for dyspepsia in 1981. Gastroscopies with stepwise biopsies were performed on all the patients initially and after an interval of 10 years., Results: Nine per cent of the patients (9/96) had features of lymphocytic gastritis in gastric biopsy at the first examination, and 12.5% (12/96) at the second examination; 7/9 patients (78%) had persistent lymphocytic gastritis during the follow up; in two the diagnostic features of lymphocytic gastritis had disappeared, and five had a new diagnosis of lymphocytic gastritis at the second examination. At the second examination 9/12 lymphocytic gastritis patients (75%) were H pylori positive histologically, while all had specific antibodies to H pylori. The lymphocytic gastritis patients had higher grades of gastritis (p = 0.009), neutrophilic and eosinophilic granulocytes, mononuclear inflammatory cells, and foveolar hyperplasia in the corpus mucosa, but smaller numbers of H pylori, than the H pylori positive patients without lymphocytic gastritis. The appearance of lymphocytic gastritis during the 10 year interval was associated with increases in the grades of corpus gastritis and neutrophilic granulocytes (p = 0.043 for both). During the follow up, the patients with lymphocytic gastritis, but not the H pylori positive patients without lymphocytic gastritis, appeared to have a significant increase in the grade of intestinal metaplasia in the corpus mucosa (p = 0.043)., Conclusions: In some patients H pylori may cause a gastritis that predominates in the corpus and is associated with an increase in the intraepithelial lymphocyte count. This form of gastritis may cause progression of intestinal metaplasia.

Lymphocytic gastritis and primary gastric lymphoma are rare conditions with unknown aetiology. It has recently been suggested that Helicobacter pylori has a role in the pathogenesis of both of them. The occurrence of lymphocytic gastritis and H pylori was studied in a series of patients with primary gastric lymphoma. The cases of primary gastric lymphomas (n = 35) diagnosed in years 1970-1993 were identified. The specimens of 22 cases contained gastric mucosa sufficiently so that the number of intra-epithelial lymphocytes, severity of gastritis, and occurrence of H pylori could be studied. Lymphocytic gastritis was detected in seven of 22 patients (32%), and in most cases both in antral and body mucosa. Atrophy of the body glands was significantly more severe in lymphocytic gastritis patients. H pylori was detected in 13 of all 22 patients (59%); two of seven lymphocytic gastritis patients (29%), and 11 of 15 (73%) of patients without lymphocytic gastritis were H pylori positive. Patients with gastric lymphoma have significantly increased prevalence of lymphocytic gastritis. Rarity of H pylori in these patients might be connected with atrophic changes in body mucosa. Further studies are needed to show the significance of lymphocytic gastritis as a precursor of gastric lymphoma.

Objectives: Simpler, effective therapies to treat Helicobacter pylori infection are greatly needed. Omeprazole co-therapy apparently enhances effectiveness of some antimicrobials. Our objective in this study was to determine whether the apparent additional benefit provided by omeprazole to amoxicillin therapy could be equaled by a high dose of ranitidine plus sodium bicarbonate., Methods: In a prospective randomized trial, we tested 1 g amoxicillin b.i.d. with either omeprazole 20 mg b.i.d., or high dose ranitidine (900 and 1800 mg) plus sodium bicarbonate tablets 650 t.i.d. (with meals) for 14 day., Results: Fifty-two patients with documented H. pylori infection and peptic ulcer completed therapy. The cure rate with omeprazole and amoxicillin was poor (46%), with the 95% confidence interval (CI) = 25-67%. Ranitidine plus sodium bicarbonate was also poor (39% cure) with the 95% CI = 21.5-59% (p > 0.57). Average compliance was more than 92% for all three groups. Side effects were experienced in only two patients (stomatitis and mild diarrhea)., Conclusion: Neither the omeprazole nor ranitidine plus bicarbonate plus amoxicillin therapies used here can be recommended for treatment of H. pylori infection.

Background: Helicobacter pylori seems to be the commonest cause of chronic gastritis, but the natural course of H. pylori-associated gastritis is largely obscure., Methods: We present a histologic follow-up of 39 patients with H. pylori-positive gastritis. Gastroscopies with stepwise biopsies were performed in all the patients at an interval of 10 years., Results: Of the patients 87% (34/39) had a persistent infection and showed a significant decrease in the grades of antral gastritis, eosinophilic granulocytes, corpus eosinophilic granulocytes, and foveolar hyperplasia and a significant increase in the grade of corpus neutrophilic granulocytes. The quantities of H. pylori as estimated histologically did not change significantly during the follow-up period in patients with a persistent infection. In the five other patients (13%) the H. pylori infection had apparently disappeared spontaneously, and this was accompanied by decreases in the amount of inflammatory cells in the gastric mucosa., Conclusions: H. pylori infection in the gastric mucosa is chronic and may be associated with both regressive and progressive histologic changes. Spontaneous healing of H. pylori infection is possible and is associated with partial resolution of the inflammatory changes in the gastric mucosa.

Background: The course of gastric ulcer disease and its relations to certain indicators of inflammation and Helicobacter pylori in the gastric mucosa were examined in a 10-year follow-up., Methods: Thirty-three patients with gastric ulcer were examined endoscopically with biopsies in 1981-82 and invited for re-examination in 1991-92. Twenty-one of them were able to comply with the invitation. A gastroscopy with biopsies was performed on each of these, and the results were compared with those of age- and sex-matched control patients with non-ulcer H. pylori-positive gastritis., Results: All the patients were H. pylori-positive at the first examination and had a persistent infection at the second examination, if they had not undergone a gastric resection. Thirteen patients had a non-operated stomach at the second examination. The grades of gastritis and intestinal metaplasia in the antrum at the second examination were significantly higher in the ulcer patients than in the controls (p = 0.009 and p = 0.04, respectively). Eosinophilic granulocytes in both the antral and the corpus mucosa had decreased significantly in the controls (p = 0.002 and p = 0.04, respectively) but not in the ulcer patients., Conclusions: The results suggest that the course of ulcer-associated H. pylori-positive gastritis is different from that of non-ulcer-associated H. pylori-positive gastritis and that abnormal eosinophilic infiltration persists in patients with gastric ulcer.

Little is known of the function of the T cells in the inflammatory infiltrate in Helicobacter pylori associated gastritis. This study thus measured T cell in vivo activation by enumerating the frequency of interferon gamma (IFN gamma) and interleukin 4 (IL 4) secreting cells isolated from the gastric antral mucosa in patients with or without gastritis and in H pylori positive and negative gastritis. Fifty four samples were examined for cytokine secretion. Four antral biopsy specimens from each patient (n = 51) were taken during diagnostic endoscopy. One was used to estimate histological gastritis and the presence of H pylori, and three of the samples were used to isolate T cells by enzymatic digestion. IFN gamma and IL 4 secreting cells were enumerated by ELISPOT. Thirty four samples had gastritis and 79% of those were H pylori positive. None of the samples from non-inflamed mucosa had H pylori. The numbers of IFN gamma secreting cells per 10(5) T cells were higher in gastritis than in normal mucosa (145 v 20 IFN gamma spots, p < 0.01), and higher in H pylori negative than H pylori positive gastritis (371 v 110 IFN gamma spots, p < 0.05). The frequencies of IL 4 secreting cells did not differ between gastritis and non-inflamed mucosa. In conclusion, there is an increase in IFN gamma secreting cells but not in IL 4 secreting cells in H pylori positive and negative gastritis. It is not known if this TH1 type reaction has a pathogenetic or protective role.

Background: Azithromycin is new acid-stable macrolide that achieves 10- to 40-fold higher tissue levels than erythromycin after oral dosing. Important to note, the tissue half-life of azithromycin is measured in days instead of hours., Method: We evaluated two new triple therapies for Helicobacter pylori infection in which azithromycin was substituted for metronidazole either as 250 mg b.i.d. or t.i.d. along with tetracycline 500 mg q.i.d. and bismuth subsalicylate 2 tablets q.i.d. for 14 days. H. pylori status was determined by histology before and 6 wk or more after therapy., Results: Thirty men with documented H. pylori peptic ulcers completed therapy. Twenty-one also received ranitidine (300 mg in the evening) along with the antimicrobial therapy. H. pylori infection was successfully treated in 15 (50%) (95% CI = 31-69%). The cure rate was significantly higher with the 250-mg-t.i.d.-azithromycin dosage regime (83%) (95% CI = 52-98%) compared to the 250-mg-b.i.d.-dosage regime (28%) (95% CI = 10-53%) (p < 0.01). Troublesome side effects were experienced by the majority of those receiving azithromycin t.i.d., Conclusion: We conclude that although 750 mg or more of azithromycin might eventually be able to replace metronidazole or clarithromycin in standard triple therapy, additional studies are required to identify a regime that is both effective and tolerable.

Background: More convenient therapies are needed to treat Helicobacter pylori infection successfully. Clarithromycin and amoxycillin are effective against H. pylori both in vivo and in vitro. Recent success with a high dose amoxycillin-metronidazole combination therapy led us to evaluate clarithromycin-amoxycillin dual therapy for H. pylori infection., Methods: We tested the combination of clarithromycin 500 mg t.d.s. with meals plus amoxycillin 750 mg t.d.s. with meals for 10 days for its effect on H. pylori infection in 29 patients with documented H. pylori peptic ulcers. There were 27 men and 2 women, ranging in age from 23 to 77 years. H. pylori and ulcer status were evaluated at entry and at least 4 weeks after ending antimicrobial therapy. For ulcer healing, ranitidine 300 mg was given each evening for 6 weeks. H. pylori status was determined by CLOtest and histology., Results: H. pylori infection was cured in 86% (95% CI = 78-99%). Compliance averaged 93% by pill count. Ten patients (34%) experienced mild side effects: eight reported dysgeusia and two had mild diarrhoea; none discontinued therapy because of side effects., Conclusion: We conclude that dual therapy with clarithromycin and amoxycillin is a safe and effective alternative regimen for the successful treatment of H. pylori infections.

The relationship between different features of gastric mucosal inflammation, intragastric pH and serum gastrin concentration and the distribution and quantity of Helicobacter pylori was studied in a series of 107 dyspepsia patients. H. pylori was identified in 62 cases (59%), and its presence was associated with increased amounts of mononuclear inflammatory cells and neutrophilic and eosinophilic leucocytes in both the antrum and the corpus. The number of H. pylori in the antral mucosa was significantly associated with the quantity of mononuclear inflammatory cells. It was also associated with glandular atrophy in antral mucosa, so that slight and moderate glandular atrophy were significantly more common in cases with abundant H. pylori. Intragastric pH and serum gastrin concentration were inversely related to the number of H. pylori in both the antral and corpus mucosa. H. pylori positive patients were also divided into groups according to proportions of H. pylori in the antral and corpus mucosa. In 5 of these patients (8%) the bacteria were present only in the corpus, and this group had a significantly more pronounced degree of glandular atrophy in the corpus mucosa, higher intragastric pH and a higher serum gastrin concentration than the other H. pylori positive patients. The other patients with a higher corpus H. pylori than antral H. pylori score (n = 25; 34%) also had a significantly higher intragastric pH and serum gastrin concentration than those with a corpus H. pylori score lower than or equal to the antral score, while the latter had more severe inflammation in the antral mucosa and a lower intragastric pH and serum gastrin concentration. The results suggest that inflammation in the antrum forms a favourable environment for H. pylori, while atrophy of the corpus glands, being connected with increased pH, leads to a diminished amount of H. pylori. They thus support the view that proliferation of H. pylori is dependent on acid produced by the corpus mucosa.

Helicobacter pylori-induced in vitro stimulation of mononuclear cells was characterized by measuring DNA synthesis response, interferon-gamma (IFN-gamma) secretion and the number of immunoglobulin-secreting cells. The strength of these responses was measured in 51 subjects comprising 36 dyspeptic patients from the Gastroenterological Unit and 15 members of the laboratory staff. Nineteen subjects had antibodies to H. pylori and 32 did not. The responses were compared with respect to H. pylori antibody status. Positive stimulation of DNA synthesis (stimulation index greater than 2) was obtained in 96% of the subjects, and the bacterium induced IFN-gamma secretion in all of them. The induction of immunoglobulin-secreting cells revealed B cell in vitro stimulation. The antibody-positive subjects had a tendency to synthesize less DNA (P not significant) and secrete less IFN-gamma (P less than 0.05) in response to H. pylori than did the antibody-negative ones, but the differences were not marked. The results show that the whole H. pylori bacterium stimulates mononuclear cells. The nature of the stimulation is not yet characterized (non-specific versus specific).