Helicobacter Pylori cagA-positive Strains Research Articles

Colonization with cagA-positive Helicobacter pylori strains in intestinal metaplasia of the esophagus and the esophagogastric junction.

Recent studies indicate that colonization with cagA-positive Helicobacter pylori (H. pylori) strains may protect against gastroesophageal reflux disease (GERD) and its complications, but the role of cagA in the etiology of Barrett's esophagus has so far been poorly investigated. The pathogenesis of intestinal metaplasia (IM) at an endoscopically normal esophagogastric junction (EGJ) is still unclear, and the role of the H. pylori virulence factor cagA in it has not been investigated. The aim of our study was to assess the relationship between H. pylori and cagA-positive H. pylori in particular and IM at an endoscopically normal EGJ and Barrett's esophagus. Serum samples were obtained from 62 patients without IM, 43 patients with IM at an endoscopically normal junction, and 51 patients with Barrett's esophagus. IM was defined as presence of goblet cells with positive staining with Alcian blue. The prevalence of H. pylori and cagA was investigated by assessment of IgG antibody levels as determined by ELISA. The overall H. pylori prevalence was 59% (92/156), and the cagA prevalence was 29% (46/156). Although 63% (39/62) of IM negative subjects and 74% (32/43) of those with IM at the junction were H. pylori positive, only 41% (21/51) of Barrett's patients tested positive. The differences between the IM negative and the Barrett's group (p = 0.02) and between IM at the junction and Barrett's were significant (p = 0.002). The relative cagA prevalence (percentage with cagA positivity and H. pylori positivity) was 56% (22/39) in patients who were IM negative, 59% (19/32) in those with IM at the junction, and 24% (5/21) in those with Barrett's. The prevalence of anti-CagA was significantly lower in patients with Barrett's esophagus compared with patients who were IM negative (p = 0.002) and those who had IM at the junction (p < 0.001). No difference in cagA prevalence was seen between the latter groups. These findings are in line with the concept that H. pylori and cagA-positive strains in particular protect against the development of Barrett's esophagus. In contrast, our findings do not support the theory that IM at an endoscopically normal esophagogastric junction is associated with H. pylori or cagA-positive strains. IM at the junction and Barrett's esophagus seem to have different etiologies.

The lack of influence of CagA positive Helicobacter pylori strains on gastro-oesophageal reflux disease.

Helicobacter pylori infection of the gastric mucosa may influence gastro-oesophageal reflux disease (GORD). The protein of cytotoxin associated gene A (CagA) is assumed to be a virulence factor of H. pylori. CagA positive strains may induce severe gastroduodenal peptic ulcer disease. The aim of this study was to evaluate the association between H. pylori strains expressing CagA and GORD. Nine hundred and thirty patients were examined by endoscopy. Antral and corpus biopsies for the urease test and serum samples for the detection of IgG antibodies to CagA were taken. Serum samples were assayed by using the western blot technique. The results from 811 patients were analysed statistically. This study population consisted of 264 H. pylori infected patients (264/811, 32%). The H. pylori prevalence was 33% (89/266) in patients with reflux oesophagitis and did not differ from those patients without oesophagitis (175/545, 32%). In contrast, patients with Barrett's oesophagus showed a significantly lower prevalence of H. pylori infection than the other three groups (8/35, 23%). There was no significant influence of CagA, as one of the H. pylori virulence factors, on GORD. Antibodies against CagA were slightly, but insignificantly, more frequent in patients with oesophagitis (55/89, 62%) than in patients without oesophagitis (94/175, 54%). In a large cohort of GORD patients no significant difference in the prevalence of H. pylori in patients with and without GORD was found. In addition, there is no correlation between patients carrying CagA positive strains and development of reflux oesophagitis. However, in the case of histopathologically proven Barrett's oesophagus the prevalence of H. pylori was significantly lower. The influence of CagA positive strains on oesophageal mucosa is discussed.

Infection by CagA-positive Helicobacter pylori strains in patients with ischemic heart disease: prevalence and association with exercise-induced electrocardiographic abnormalities.

The role of H. pylori infection in increasing the risk of ischemic heart diseases (IHD) is still debated. We determined serologically the prevalence of overall H. pylori and CagA-positive H. pylori infection in 63 consecutive patients with IHD and 189 gender- and age-matched controls. We also determined in patients the influence of the infection and the CagA serological status on the results of an exercise ECG test and other parameters considered possible variables that may enhance the risk of IHD. The prevalence of H. pylori infection in patients and controls was 79.3% and 73.0%, respectively (P = 0.403) and that of CagA-positive H. pylori infection was 69.8% and 42.3%, respectively (P = 0.0002). The scores of the ECG S-T segment and T-wave abnormalities in the course of an exercise ECG in uninfected patients and in patients infected by CagA-negative and CagA-positive H. pylori strains were (mean +/- SD): 1.59 +/- 0.67, 1.92 +/- 0.64, and 2.19 +/- 0.70, respectively; (P = 0.011, 95% confidence limits of difference 0.15-1.07, CagA-positive infected vs uninfected patients). There was no intergroup difference in the levels of peripheral white blood cells, glucose, cholesterol, triglycerides, creatinine, and systolic and diastolic pressure. In conclusion, genetic heterogeneity of H. pylori could possibly explain some conflicting results concerning the association of H. pylori infection with IHD. Coronary vessels of IHD patients infected by CagA-positive H. pylori strains may be damaged more severely than those of uninfected patients.

Gastric permeability is not increased in children colonized by CagA-positive strains of Helicobacter pylori

Background. Sucrose permeability has been used as a marker to detect gastric lesions in children. As CagA status of Helicobacter pylori is an important factor in determining the evolution of the gastric lesion, CagA-positive strains being more frequently associated with severe mucosal lesions, the aim of this study was to determine the prevalence of CagA-positive strains in Helicobacter pylori-colonized children and to evaluate whether the sucrose permeability test might discriminate between colonization by CagA-positive or negative strains. Patients and methods. A series of 38 children (11.1 ±3.6 years] who required upper endoscopy for diagnostic purposes were included in the study. Endoscopy was carried out after the sucrose permeability test, and gastric biopsies were obtained for histologic examination, Helicobacter pylori detection by Giemsa staining and CLO-test, and determination of CagA status of the colonizing Helicobacter pylori strains by polymerase chain reaction. Results. Helicobacter pylori was detected in 26 subjects (68.4%) and of these, 16 (61.5%) were colonized by CagA-positive strains. The intensity of the histologic findings was significantly associated with the presence of Helicobacter pylori and with CagA status of the infecting strains ( χ 2=21.2, p=0.0017). However, no significant difference in the urinary excretion of sucrose between children not colonized and children with CagA-negative or positive strains was observed (0.027% (0.012-0.035%); 0.027% (0.016-0.047%) and 0.026% [0.016-0.038], median [range], respectively; Kruskal-Wallis analysis of variance F=0.75, p=O.69). Conclusions. These results indicate that in Chile, about 60% of the Helicobacter pylori infected children are colonized by CagA-positive strains, in association with more intense lesions of the gastric mucosa, but that gastric permeability to sucrose does not discriminate between colonization by CagA-negative and positive strains of Helicobacter pylori.

Functional Dyspepsia is Associated with cagA-positive Helicobacter pylori Strains

Background: The antigen CagA can be used as a marker for virulence of Helicobacter pylori. It is tempting to assume that H. pylori strains positive for cytotoxin-associated gene A (cagA) could be responsible for functional dyspepsia. A cross-sectional study was performed in patients presenting with functional dyspepsia to correlate the clinical presentation with the presence of cagA-positive and -negative H. pylori strains. Methods: Consecutive patients referred for endoscopy were studied. An inclusion criterion was the absence of any endoscopic abnormality. Biopsy specimens were obtained from the gastric antrum for HE and immunoperoxidase stain, rapid urease test, and culture. A serum sample was taken for detection of IgG antibodies against H. pylori as well as CagA. A validated questionnaire of 14 questions regarding the upper gastrointestinal tract was used for assessment of the clinical presentation. Nine questions were scored on a 5-point Likert scale. Results: 422 patients were included, 222 were H. pylori-positive, the remaining 200 were H. pylori-negative. Mean symptom score in patients with cagA-positive strains was significantly higher than in patients with cagA-negative strains. No difference was present if cagA-negative patients were compared with H. pylori-negative dyspeptics. Four different complaints were more prevalent in the cagA-positive patients compared with cagA-negatives. When cagA-positive patients were compared with H. pylori-negative dyspeptics, seven complaints were significantly more prevalent in cagA-positives; when cagA-negatives were compared this number was only two. Conclusions: Functional dyspeptics with cagA-positive H. pylori strains have more dyspeptic symptoms and higher symptom scores than patients with cagA-negative H. pylori strains as well as H. pylori-negative functional dyspeptics.

Helicobacter pylori CagA-positive Strains Affect Oxygen Free Radicals Generation by Gastric Mucosa

Background:Helicobacter pylori plays a key role in production of reactive oxygen metabolites (ROMs). However, the importance of virulent CagA-positive H. pylori strains remains to be determined. The aim of this study was to assess ROMs production in gastric biopsies of patients infected by H. pylori. Results were correlated to CagA status and acute inflammatory infiltration. Methods: Patients undergoing gastroscopy were enrolled. H. pylori infection was assessed by histology and 13C urea breath test. CagA status was assessed through serology. ROMs were assayed in gastric biopsies by luminol-enhanced chemiluminescence (CLS). Gastric mucosal inflammation was histologically graded and neutrophils were individually counted. Macroscopical damage was scored according to a modified Lanza score. Results: 40 out of 60 patients evaluated were H. pylori (HP) positive. Of the 40 infected patients, 24 were CagA-positive. CLS emission was significantly higher in HP-CagA-positive patients than in HP-CagA-negatives and uninfected. ROMs production showed a significant correlation to neutrophil infiltrate in all groups. Conclusions: Gastric mucosa of patients infected by HP-CagA-positive strains is characterized by a higher generation of ROMs and by greater neutrophil counts than that observed in HP-CagA-negative subjects. Since ROMs production is associated with DNA oxidative damage, a long-term stimulation by these strains might be relevant in the pathogenesis of gastric malignancies. Assessment of CagA status might be useful to discriminate patients in which H. pylori eradication is advisable.

Caga-positive strains of Helicobacter pylori may protect against Barrett’s esophagus

OBJECTIVE: Helicobacter pylori (H. pylori) colonization is associated with chronic gastritis, peptic ulcer disease, and adenocarcinoma of the distal stomach. However, the role of H. pylori strain variation in complicated gastroesophageal reflux disease, especially Barrett’s esophagus, is unknown. Therefore, the aim of this study was to evaluate the prevalence of colonization by cagA + and cagA − H. pylori strains in the spectrum of gastroesophageal reflux disease, including Barrett’s esophagus. METHODS: A total of 251 patients undergoing endoscopy were categorized into four groups: controls, patients with gastroesophageal reflux disease alone, and patients with short- and long-segment Barrett’s esophagus. All patients underwent upper endoscopies with biopsies and serum collections. H. pylori and degree of mucosal inflammation in gastric biopsies were assessed and serological assessment made for H. pylori and cagA status. RESULTS: The overall prevalence of H. pylori colonization in the study population was 35% (95% confidence interval = 29.5–41.4%) which did not differ significantly among the groups. However, colonization by cagA + H. pylori strains was significantly more prevalent among controls (11/25; 44%) and patients with gastroesophageal reflux disease (13/36; 36%) than in patients with short-segment (2/10; 20%) or long-segment Barrett’s esophagus (0/18; 0%). Patients with Barrett’s esophagus were less likely to be colonized by cagA + H. pylori strains than reflux patients without Barrett’s esophagus (odds ratio = 0.27, 95% confidence interval = 0.11–0.67, p = 0.004). CONCLUSIONS: Colonization by cagA + H. pylori strains may be protective against the formation of short- and long-segment Barrett’s esophagus and its malignant complications.

Helicobacter pylori and dyspepsia: a population-based study of the organism and host.

The role of Helicobacter pylori (HP) infection in dyspepsia in the absence of peptic ulcer remains controversial. Specific attributes of the organism or the host response may be important. We aimed to determine whether HP infection overall, CagA status, serum gastrin, or serum pepsinogen levels are associated with dyspepsia in the community. A self-report bowel disease questionnaire was mailed to a random sample of Olmsted County, Minnesota residents, aged 20-50 yr. All respondents who reported symptoms of dyspepsia or irritable bowel syndrome (cases) and all respondents without significant GI symptoms (controls) were invited to participate (n = 260). They were each assessed by a physician and their medical records reviewed. Serum was obtained to measure HP and CagA antibodies, pepsinogen I and II levels, and basal serum gastrin using validated assays. Of the 148 (57%) subjects who agreed to participate, 36 had dyspepsia (17 had ulcer-like dyspepsia), 35 had irritable bowel syndrome (IBS) without dyspepsia, and 77 were asymptomatic. The proportion who were seropositive for HP were 17% in dyspepsia (24% in ulcer-like dyspepsia), 20% in IBS, and 12% in asymptomatic controls. HP was not associated with dyspepsia, ulcer-like dyspepsia, or IBS after adjusting for age. Pepsinogen levels and serum gastrin were not associated with any of the conditions studied. However, CagA antibody positivity was associated with IBS (p < 0.05), and a borderline statistically significant association with dyspepsia was detected (p = 0.08). In this community, HP infection overall does not seem to explain dyspepsia, although the role of CagA-positive HP strains deserve further study.

Helicobacter pylori and dyspepsia: a population-based study of the organism and host

OBJECTIVE: The role of Helicobacter pylori (HP) infection in dyspepsia in the absence of peptic ulcer remains controversial. Specific attributes of the organism or the host response may be important. We aimed to determine whether HP infection overall, CagA status, serum gastrin, or serum pepsinogen levels are associated with dyspepsia in the community. METHODS: A self-report bowel disease questionnaire was mailed to a random sample of Olmsted County, Minnesota residents, aged 20–50 yr. All respondents who reported symptoms of dyspepsia or irritable bowel syndrome (cases) and all respondents without significant GI symptoms (controls) were invited to participate (n = 260). They were each assessed by a physician and their medical records reviewed. Serum was obtained to measure HP and CagA antibodies, pepsinogen I and II levels, and basal serum gastrin using validated assays. RESULTS: Of the 148 (57%) subjects who agreed to participate, 36 had dyspepsia (17 had ulcer-like dyspepsia), 35 had irritable bowel syndrome (IBS) without dyspepsia, and 77 were asymptomatic. The proportion who were seropositive for HP were 17% in dyspepsia (24% in ulcer-like dyspepsia), 20% in IBS, and 12% in asymptomatic controls. HP was not associated with dyspepsia, ulcer-like dyspepsia, or IBS after adjusting for age. Pepsinogen levels and serum gastrin were not associated with any of the conditions studied. However, CagA antibody positivity was associated with IBS ( p < 0.05), and a borderline statistically significant association with dyspepsia was detected ( p = 0.08). CONCLUSIONS: In this community, HP infection overall does not seem to explain dyspepsia, although the role of CagA-positive HP strains deserve further study.

Intestinal metaplasia of the cardia and infection with caga-positive Helicobacter pylori strains in gastroesophageal reflux disease

Intestinal metaplasia of the cardia and infection with caga-positive Helicobacter pylori strains in gastroesophageal reflux disease

Mucosal humoral immune response to CagA shows a high prevalence in patients with gastric MALT-type lymphoma.

In the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT)-type lymphoma, CagA-positive Helicobacter pylori strains have been suspected of making a significant contribution. To investigate this hypothesis in more detail, the mucosal humoral immune response of 15 patients with gastric MALT-type lymphoma was examined in the tumor and in the tumor-free gastritis of the same patient. Mononuclear cells from different sites (antrum, corpus, lymphoma) were cultured. Culture supernatant and serum of the same patient were used for immunodetection of CagA. All patients displayed an immune response to CagA in the tissue-culture supernatants. Although the humoral immune response in the tumor was restricted to a very few H. pylori antigens, antibodies directed against CagA protein were found in most patients. The immune response to CagA in nearly all lymphoma patients--not only in the serum, but also in the mucosa, including the tumor site--support the hypothesis that CagA is involved in the pathogenesis of gastric MALT-type lymphoma.

Coexpression of interleukin-8 and inducible nitric oxide synthase in gastric mucosa infected with cagA+ Helicobacter pylori.

The cagA-positive Helicobacter pylori strains are thought to be able to induce interleukin-8 expression and to be associated with gastroduodenal diseases. Inducible nitric oxide synthase (iNOS) may be involved in inflammatory pathogenesis. Our aim was to investigate the interrelationships between cagA and the expression of interleukin-8 and iNOS messenger RNAs, and with the type and degree of inflammation in gastric mucosa. In biopsies from 108 Chinese patients, the cagA, 16S rRNA, interleukin-8, and iNOS mRNAs were analyzed using reverse-transcription polymerase chain reaction. Specimens infected with cagA-positive strains had significantly more severe infiltration by mononuclear and polymorphonuclear leukocytes and more frequently expressed interleukin-8 and iNOS mRNAs than those infected with cagA-negative strains. iNOS and interleukin-8 mRNAs were significantly more frequently expressed together in the specimens with moderate or severe inflammation than in those with normal mucosa or mild inflammation. Our data suggest that interleukin-8 and excess nitric oxide play important roles in the pathogenesis of H. pylori-associated gastroduodenal diseases.

Serologic detection of CagA positive Helicobacter pylori strains predicts the presence of peptic ulcer in young dyspeptic patients

Background: Helicobacter Pylori infection has been strongly associated with upper gastrointestinal (GI) disease, especially duodenal ulcer. Endoscopy or contrast radiography is needed to diagnose and appropriately manage peptic ulcer disease. These diagnostic procedures, however, are time consuming and expensive; endoscopy is invasive and contrast radiography cannot help in the diagnosis of H pylori infection. Our aim was to examine in a prospective study the relation between serologic detection of cytotoxic associated gene (CagA) H pylori strains and endoscopic findings among young dyspeptic patients to determine whether this noninvasive test can help differentiate patients with from those without ulcers. Methods: One hundred patients younger than 45 years with dyspepsia referred for upper GI endoscopy were included in the study. During endoscopy antral biopsy specimens were obtained for the rapid urease test and histologic examination. At histologic examination gastritis was graded from 0 (normal histologic features) to 3 (severe gastritis). After endoscopy blood was obtained for serologic determination of CagA status. Results: Among the 100 patients 56 were H pylori positive and 44 were H pylori negative. In the group of 56 H pylori –positive patients 36 (64.3%) had peptic ulcers and 20 (35.7%) did not. Among patients with peptic ulcer 34 of 36 (94.4%) were CagA positive and 2 (5.6%) were CagA negative. The respective values for the group of patients without ulcers were 9 of 20 (45%) and 11 of 20 (55%). The difference in the proportion of CagA-positive subjects between the group with and that without peptic ulcer was highly significant ( p < 0.0001). Conclusions: Among young patients with dyspepsia, CagA seropositivity is highly associated with duodenal ulcer at endoscopy. (Gastrointest Endosc 1999;50:511-5.)

CagA and Cytotoxicity of Helicobacter pylori Are Not Markers of Peptic Ulcer in Japanese Patients

The infection with cagA-positive Helicobacter pylori strains is reported to be associated with peptic ulcer disease in developed countries, but it is controversial in Asia. To investigate the relationship between the virulence factors of H. pylori and peptic ulcer disease in Japan, we compared these between ulcer and nonulcer patients. Seventy-four strains of clinically isolated H. pylori obtained from 22 gastric ulcer (GU), 23 duodenal ulcer (DU), and 29 chronic gastritis (CG) patients were studied. The presence of vacA and cagA gene was examined by polymerase chain reaction method using two different primer sets. We evaluated the proliferation-inhibiting and lethal cytotoxicity of culture supernatants using the alamarBlue assay. The vacA gene was identified in all strains by the original primers. S1 strains were found in 90.9% (20/22) from GU, 95.7% (22/23) from DU, and 96.6% (28/29) from CG patients. The prevalence of cagA gene determined by the first, and second primers was 90.9% (20/22), 90.9% (20/22) in strains from GU, 87.0% (20/23), 91.3% (21/23) from DU, and 86.2% (25/29), 89.7% (26/29) from CG patients, respectively. The supernatant showed cytolethal effect in 95.5% (21/22) of strains from GU, in 100% (23/23) from DU, and in 93.1% (27/29) from CG patients. There was no significant difference in the prevalence of the virulence factors between H. pylori strains isolated from patients with peptic ulcers and those with chronic gastritis. These results indicate that cagA gene status and the proliferation-inhibiting and lethal cytotoxicity of supernatant are not reliable markers of ulcerogenicity of H. pylori in Japanese patients.

Risk for developing gastric carcinoma in patients colonized by cagA positive Helicobacter pylori strains

Risk for developing gastric carcinoma in patients colonized by cagA positive Helicobacter pylori strains

Association of CagA-Positive and CagA-Negative Helicobacter pylori Strains with Patients' Symptoms and Gastritis in Primary Care Patients with Functional Upper Abdominal Complaints

Background: CagA-positive Helicobacter pylori strains have been reported to be associated with peptic ulcer or malignancy more often than cagA-negative strains. Less is known about the relation of H. pylori serology (CagA-negative or CagA-positive) to histologic changes in the stomach of patients with functional upper abdominal complaints. The association of H. pylori status with patient symptoms or with different subgroups of non-organic dyspepsia is also obscure. In the present study patients' symptoms and their relation to H. pylori serology (H. pylori-negative, H. pylori-positive but CagA-negative, and H. pylori-positive and CagA-positive) were evaluated in general practice patients who had functional upper abdominal complaints. The association of H. pylori serology with different symptom-based subgroups of functional upper abdominal complaints was also assessed. The severity and activity of inflammation and the presence of atrophy and intestinal metaplasia in the antrum and body were evaluated and compared with H. pylori status. Methods: Four hundred consecutive unselected dyspeptic patients in primary care were investigated by means of gastroscopy, upper abdominal ultrasound, laboratory screening including H. pylori and CagA serology, and other examinations if needed. Of these patients 193 with functional upper abdominal complaints were enrolled in this study. Results: Of the study patients 87 (45%) were H. pylori-negative, 70 (36%) were H. pylori- and CagA-positive, and 36 (19%) were H. pylori-positive but CagA-negative. There were no differences in the occurrence of any dyspeptic symptoms between H. pylori-related subgroups. Nor was there an association between H. pylori status and symptom-based subgroups in our study patients. Inflammation of the stomach was related to H. pylori infection, but CagA-seropositive patients did not have moderate or severe inflammation more often than CagA-seronegative ones. CagA-seropositive patients with functional upper abdominal complaints did not have atrophic changes or intestinal metaplasia in the stomach more often than those who were CagA-negative. Conclusions: H. pylori or more specific CagA serology is not associated with any specific symptom profile of dyspepsia or with any symptom-based subgroups in patients with functional upper abdominal complaints in primary care. The study patients with CagA seropositivity did not have more severe histologic changes in the stomach than the patients who were H. pylori-seropositive but CagA-seronegative.

Analysis and typing of the vacA gene from cagA-positive strains of Helicobacter pylori isolated in Japan.

Approximately 50% of Helicobacter pylori strains produce a cytotoxin that is encoded by vacA and that induces vacuolation of eukaryotic cells. Mosaicism in vacA alleles was reported, and there are three different families of vacA signal sequences (s1a, s1b, and s2) and two different families of middle-region alleles (m1 and m2). In addition, the vacA genotype of a strain is associated with its cytotoxin phenotype and its capacity to induce peptic ulceration. To clarify the strain diversity of H. pylori in Japan, 87 Japanese clinical isolates of H. pylori (40 from patients with chronic atrophic gastritis, 25 from patients with duodenal ulcer, 16 from patients with gastric ulcer, 3 from patients with both duodenal and gastric ulcers, and 3 from patients with intestinal type gastric cancer) were characterized by vacA typing by PCR and DNA sequencing. Eighty-four of the 87 isolates were s1a/m1, one was s1b/m1, and two could not be typed. Moreover, all isolates in this study were cagA positive. There were no distinct differences between the cytotoxin-producing strains and cytotoxin-nonproducing strains within the 0.73-kb middle region. Japanese strains were highly homologous, with more than 96% identity in this region, in which maximum divergence has been reported. In addition, there were no associations between the specific vacA types and the level of in vitro cytotoxin activity or the clinical consequences. These results indicate that the cagA-positive, s1a/m1-type strains are common in Japan, regardless of the vacA phenotype or clinical outcome.

High Prevalence of the CagA-positive Helicobacter pylori Strains in Japanese Asymptomatic Patients and Gastric Cancer Patients

Background: Several studies have shown that infection of Helicobacter pylori strains possessing cagA is associated with atrophic gastritis and gastric cancers. Method: In 58 pairs of early gastric cancer patients and sex- and age-matched controls, isolated H. pylori strains were tested for possession of cagA. The presence of atrophic gastritis was also examined. Results: Proportions of cagA-positive strains were 100% in cancer patients and 92.3% in controls. Atrophic gastritis was seen in 96.7% and 95.8% of cancer and control patients in whom cag4-positive strains (NS) were detected. However, it was seen in only 20% of H. pylori-negative control patients (P < 0.01). Conclusions: The present results do not suggest any specific association between cagA -positive strains and gastric cancer. However, frequent prevalence of cagA-positive strains might be associated with the high incidence of atrophic gastritis in Japanese populations.

Helicobacter pylori infection enhances mucosal interleukin-1 beta, interleukin-6, and the soluble receptor of interleukin-2.

It is thought that Helicobacter pylori colonization of the gastric mucosa might stimulate the production of several cytokines, which might trigger and maintain the gastric inflammation associated with Helicobacter pylori infection. In the present study we evaluated interleukin-1 beta. interleukin-6, and the soluble receptor of interleukin-2 both in mucosal homogenates and in the sera of Helicobacter pylori-infected (39 cases) and uninfected (40 cases) patients to investigate whether there was any relationship between variations in cytokines and (1) the severity of Helicobacter pylori-associated gastritis or (2) CagA-positive Helicobacter pylori strains. Mucosal, but not serum levels of interleukins-1 and -6 and interleukin-2 receptor were significantly higher in infected than uninfected patients. Serum levels of Helicobacter pylori antibodies were significantly higher in infected than uninfected patients. These levels correlated with mucosal interleukin-1 beta. The degree of antral or body inflammatory grade was higher in infected than in uninfected patients; cytokines levels were higher in patients with high-grade gastritis, most of whom were Helicobacter pylori positive. Patients infected with CagA-positive strains also had higher levels of interleukin-1 beta, but not of interleukin-2 receptor or interleukin-6. In conclusion. Helicobacter pylori infection results in a local increase in interleukins-1 beta and -6 and interleukin-2 receptor associated with high-grade mucosal inflammation. Interleukin-1 beta seems to favor anti-Helicobacter pylori antibody production, and mucosal levels are enhanced mainly in patients infected with cytotoxic Helicobacter pylori strains.

Infection with cagA positive Helicobacter pylori strains increases the risk for atrophic gastritis : [formula omitted], GI. Pérez-Pérez, SGM. Meuwissen, MJ. Blaser. Free Univ Hosp, Amsterdam, The Netherlands, and Vanderbilt Univ Sch Med, Nashville TN

Infection with cagA positive Helicobacter pylori strains increases the risk for atrophic gastritis : [formula omitted], GI. Pérez-Pérez, SGM. Meuwissen, MJ. Blaser. Free Univ Hosp, Amsterdam, The Netherlands, and Vanderbilt Univ Sch Med, Nashville TN