Pylori In Gastric Mucosa Research Articles

Assessment of the Simultaneous Presence of Helicobacter Pylori in the Gastric Mucosa and Gallbladder Mucosa in Patients Suffering from Cholecystitis: a cross Sectional Study

Aim: The current study was designed to assess the simultaneous presence of H. pylori in gastric and gallbladder mucosa in the patients of acute cholecystitis or symptomatic cholelithiasis. Study design: Cross sectional study Place and duration: This study was conducted at Liaquat University Hospital Hyderabad, Pakistan from March 2020 to March 2021. Methodology: A total of 43 patients suffering from acute cholecystitis and symptomatic cholelithiasis were selected. Their age, gender, and the presence of H. pylori in the gallbladder and gastric mucosa was determined and recorded. The results were statistically analyzed by SPSS version 22. Results: Out of the 43 patients, 20 were male, and 23 were female. Recorded mean age was 54.8±9.9 years and 22 (51.2%) had acute cholecystitis and the remaining 21 (48.8%) had cholelithiasis. In the gastric mucosa, in 14 patients (32.6%) H. pylori was positive. Similarly, in the gall bladder; it was positive in 19 patients (44.2%). In 6 patients (13.9%) i.e. in 4 men and 2 women, H pylori was simultaneously present in both gallbladder and gastric mucosa. No particular relationship was observed in the H. pylori’s presence or absence in gallbladder and gastric mucosa. Conclusion: The presence of H. pylori in gallbladder plays a critical role in the gallbladder’s infection. However, its simultaneous presence in gastric mucosa is not a good standard to assess biliary diseases. Keywords: H. pylori, Cholecystitis, Cholelithiasis, Gallbladder, Gastric mucosa

Benign effects of Helicobacter pylori in gastric mucosa among symptomatic Sudanese patients

Introduction:Infection with Helicobacter pylori is a worldwide problem. It plays an important role in gastric malignancies.The pathogenesis of gastric malignancies involves multistep progression changes in gastric mucosaand the Helicobacter pylori infections is the first step in most of cases.Aim:The aims of this study were to clarify the benign changes in gastric mucosa after Helicobacter pylori infection;to evaluate the endoscopic and histological patterns of infection and to correlate endoscopic findingwith histopathological parameters.Materials and Methods:A descriptive, retrospective study was done in Soba University Hospital between January 2009 - February2013. Paraffin-embedded blocks, Giemsa and Haematoxylin and Eosin-stained slides, were obtained from50 cases of Helicobacter pylori-associated chronic gastritis and examined under light microscopy. Theclinical information and endoscopy findings were obtained from the records. The data was analyzed usingStatistical Package for Social Sciences Software.Results:The most common affected age group was between 40-60 years. The prevalence of infection was equal inmales and females. The commonest endoscopic finding was inflammation of gastric mucosa. Most patientspresented with moderate degree of colonization; 62% of patients presented with a severe degree of chronicinflammation. There was a significant statistical correlation between the degree of Helicobacter pylori colonizationand the degree of chronic inflammation (p<0.05). Most patients presented with severe degree ofactive gastritis. A significant correlation was found between the degree of chronic inflammation and degreeof activity. The prevalence of lymphoid follicles in a single biopsy specimen from antral mucosa was 36%.The dysplasia was seen in 12%; eosinophilia 8%; atrophy 8% and intestinal metaplasia in 6% of the cases.No significant correlation was found between the endoscopic findings and histological findings.Conclusion:Helicobacter pylori infection causes chronic active gastritis and it has a role in the development of lymphoidfollicles, intestinal metaplasia, atrophy and dysplasia.

Helicobacter pylori in gastric cancer: Features of infection and their correlations with long-term results of treatment.

BACKGROUND Helicobacter pylori (H. pylori) is a spiral-shaped bacterium responsible for the development of chronic gastritis, gastric ulcer, gastric cancer (GC), and MALT-lymphoma of the stomach. H. pylori can be present in the gastric mucosa (GM) in both spiral and coccoid forms. However, it is not known whether the severity of GM contamination by various vegetative forms of H. pylori is associated with clinical and morphological characteristics and long-term results of GC treatment. AIMTo establish the features of H. pylori infection in patients with GC and their correlations with clinical and morphological characteristics of diseases and long-term results of treatment.METHODSOf 109 patients with GC were included in a prospective cohort study. H. pylori in the GM and tumor was determined by rapid urease test and by immunohistochemically using the antibody to H. pylori. The results obtained were compared with the clinical and morphological characteristics and prognosis of GC. Statistical analysis was performed using the Statistica 10.0 software. RESULTS H. pylori was detected in the adjacent to the tumor GM in 84.5% of cases, of which a high degree of contamination was noted in 50.4% of the samples. Coccoid forms of H. pylori were detected in 93.4% of infected patients, and only coccoid-in 68.9%. It was found that a high degree of GM contamination by the coccoid forms of H. pylori was observed significantly more often in diffuse type of GC (P = 0.024), in poorly differentiated GC (P = 0.011), in stage T3-4 (P = 0.04) and in N1 (P = 0.011). In cases of moderate and marked concentrations of H. pylori in GM, a decrease in 10-year relapse free and overall survival from 55.6% to 26.3% was observed (P = 0.02 and P = 0.07, respectively). The relationship between the severity of the GM contamination by the spiral-shaped forms of H. pylori and the clinical and morphological characteristics and prognosis of GC was not revealed.CONCLUSIONThe data obtained indicates that H. pylori may be associated not only with induction but also with the progression of GC.

Efficacy and Gut Dysbiosis of Gentamicin-Intercalated Smectite as a New Therapeutic Agent against Helicobacter pylori in a Mouse Model.

Helicobacter pylori eradication rate with conventional standard therapy is decreasing owing to antibiotic resistance, necessitating novel antibacterial strategies against H. pylori. We evaluated the efficacy of a gentamicin-intercalated smectite hybrid (S-GM)-based treatment and analyzed fecal microbiome composition in H. pylori-infected mice. To evaluate anti-H. pylori efficacy, mice were divided into eight groups, and H. pylori eradication was assessed by a Campylobacter-like organism (CLO) test and PCR assay of H. pylori in gastric mucosa. One week after H. pylori eradication, pro-inflammatory cytokine levels and atrophic changes in gastric mucosa were examined. Stool specimens were collected and analyzed for microbiome changes. The S-GM-based triple regimen decreased bacterial burden in vivo, compared with that in untreated mice or mice treated with other regimens. The therapeutic reactions in the CLO test from gastric mucosa were both 90% in the standard triple therapy and S-GM therapy group, respectively. Those of H. pylori PCR in mouse gastric mucosa were significantly lower in standard triple therapy and S-GM therapy groups than in the non-treatment group. Toxicity test results showed that S-GM therapy reduced IL-8 level and atrophic changes in gastric mucosa. Stool microbiome analysis revealed that compared with mice treated with the standard triple therapy, mice treated with the S-GM therapy showed microbiome diversity and abundant microorganisms at the phylum level. Our results suggested that S-GM is a promising and effective therapeutic agent against H. pylori infection.

Brunner's Gland Hyperplasias and Hamartomas in Association with Helicobacter pylori.

Background The proliferative lesions of the Brunner's glands (BGs) are hyperplasia and hamartomas, and they are usually asymptomatic and very rarely diagnosed. The aetiology of these lesions is not yet clear. The aim of this study is to evaluate the clinical presentations of patients with BG hyperplasia and hamartomas and to assess the pathological features of these lesions in association with Helicobacter pylori (H. pylori). Methods Our retrospective study included patients who underwent upper gastrointestinal system endoscopy between 2010 and 2015. The hospital records of 18 patients diagnosed with hyperplasia or hamartoma of BG were reviewed for the clinical and pathological findings. Data from patients with BG lesion were compared with 37 patients who had nonspecific duodenitis as the control group. Results Female/male ratio in our study sample was 1/1. The age range was between 16 and 85 years with a mean age of 48.61. BG hyperplasia and hamartomas were found in 72.22 and 27.78% of the patients, respectively. The rate of H. pylori in gastric mucosa was 43.2% in the control group and 66.7% in the BG lesion group. In the BG lesion group, the rate of H. pylori was higher. H. pylori was identified in 60% of BG hamartomas and in 69.2% of hyperplastic BGs. Conclusion Our study demonstrated that H. pylori may play an important role in the development of BG hyperplasia and hamartomas in association with chronic gastritis and duodenitis. This is probably due to chronic irritation.

Detection of the clarithromycin resistance of Helicobacter pylori in gastric mucosa by the amplification refractory mutation system combined with quantitative real-time PCR.

The goal of this study was to evaluate the feasibility of detecting Helicobacter pylori clarithromycin resistance in gastric mucosa using the amplification refractory mutation system combined with quantitative real‐time PCR (ARMS‐PCR). Gastric mucosal specimens (150) were collected from patients who were unsuccessfully treated for H. pylori eradication. Each specimen was divided into 2 samples. One sample was used to extract genomic DNA and detect any gene mutations of H. pylori produced by ARMS‐ PCR. Sequencing was used to assess the accuracy of this method. The other sample was used to culture H. pylori. The E‐test minimum inhibitory concentration (MIC) was used to assess clarithromycin resistance. The results were compared with a paired chi‐square test to validate the coincidence rate among the 3 methods. The coincidence rate between the sequencing and ARMS‐PCR results was 98.7%, thus verifying the accuracy of ARMS‐PCR. E‐tests detected 144 clarithromycin resistance cases, including 45 sensitivity cases; the resistance rate was 70%. The coincidence rate between the results of the E‐test and ARMS‐PCR was 97.1%, and no significant difference between the 2 methods was observed. ARMS‐PCR is a simple and fast method that has high sensitivity and specificity and can be used to detect the clarithromycin resistance of H. pylori in gastric mucosa. ARMS‐PCR is expected to be used to study drug resistance mechanisms and use in assays of individual therapies for H. pylori eradication.

Feasibility of amplification refractory mutation system in fast detection of clarithromycin resistance of Helicobacter pylori in gastric mucosa

Objective To evaluate the feasibility of the combination of amplification refractory mutation system (ARMS) and quantitative real-time polymerase chain reaction (PCR) method in fast detection of clarithromycin resistance of Helicobacter pylori (H.pylori) in gastric mucosa. Methods A total of 150 gastric mucosal specimens with positive H. pylori culture were collected from the H. pylori positive patients who failed in H. pylori eradication from January to August in 2013. The drug resistant gene mutation types of H. pylori in these samples were detected by quantitative real-time PCR based on ARMS. And the accuracy was confirmed by sequencing. The clarithromycin resistance of H. pylori was determined by E-assay. Chi-square test was used for statistical analysis. Results Among 149 gastric mucosal specimens (one specimens without wild type or mutation type had been eliminated), the results of quantitative real-time PCR based on ARMS of two samples were not consistent with the results of sequencing; the consistent rate was 98.7% (147/149). Among 149 specimens with positive H. pylori culture, 104 samples (69.8%) were clarithromycin resistance. In 101 samples the clarithromycin resistance was detected by quantitative real-time PCR based on ARMS; the consistent rate was 97.1% (101/104). Both E-assay and clarithromycin resistant rate detected by E-assay or quantitative real-time PCR based on ARMS was 69.8% (104/149) and 67.8% (101/149), respectively, and the difference was not significant (χ2=0.141, P=0.932). Conclusion The combination of ARMS and quantitative real-time PCR method in fast detection of clarithromycin resistance of H. pylori in gastric mucosa is strongly feasible and highly consistent has high consistent rate with sequencing and E-assay. Key words: Helicobacter pylori; Amplification refractory mutation system; Mutation; Resistance

Elongated Helicobacter pylori in gastric mucosa of children associated with gastric disease

Two human gastric pathogens, Helicobacter pylori and Helicobacter heilmannii are apparently different genetically as well as morphologically. H. pylori have short spiral morphology while H. heilmannii is a long spiral bacterium with four or more turns. In this study, we observed elongated, spiral, Gram-negative organisms in crush smears of antral biopsies from two children with upper abdominal pain and one with celiac disease; all these biopsies were positive for rapid urease test. Histologically the children had mild to moderate gastritis. Ultra-structurally, the organisms were more elongated than H. pylori and spiral shaped with periplasmic space. They were grown on chocolate Brucella agar and colonies were identified as H. pylori biochemically and by urease gene based polymerase chain reaction. Nuclear magnetic resonance study of sonicated extracts of these organisms showed similar metabolic peaks as H. pylori. 16S-rDNA sequencing results confirmed that the isolated organisms were H. pylori. The study suggests that a morphologically different (elongated) form of H. pylori strain exists in the stomach of children and is associated with gastric pathology.

Oral Intake of N-acetyl-D-glucosamine Suppresses the Growth of Helicobacter Pylori in Gastric Mucosa of Mongolian Gerbils by Increasing Gland Mucus

Oral Intake of N-acetyl-D-glucosamine Suppresses the Growth of Helicobacter Pylori in Gastric Mucosa of Mongolian Gerbils by Increasing Gland Mucus

Helicobacter pylori infection and expressions of apoptosis-related proteins p53, ASPP2 and iASPP in gastric cancer and precancerous lesions

AimsThere has been limited information about the relations between Helicobacter pylori infection and expressions of apoptosis-related proteins p53, ASPP and iASPP in gastric cancer and precancerous lesions. MethodsH. pylori in gastric mucosa were identified by W-S staining and rapid urease test. Expression of apoptosis-related proteins P53, ASPP2 and iASPP in the gastric tissues were determined by immunohistochemistry. ResultsThe concentrations of H. pylori and expressions of p53 and iASPP in gastric carcinoma group and precancerous lesion group were higher than in benign gastric diseases group (P<0.05). The expressions of ASPP2 in gastric carcinoma and precancerous lesion group were lower than in benign gastric diseases group (P<0.05). The expressions of p53 and iASPP in H. pylori positive group were higher than in H. pylori negative group (P<0.05), whereas ASPP2 in H. pylori positive group were lower than in H. pylori negative group (P<0.05). ConclusionThere was a higher rate H. pylori infection, an increased expression of apoptosis inhibitor iASPP, and decreased expression of apoptosis stimulator ASPP2 in gastric cancer or precancerous tissues. These results suggest that H. pylori may cause gastric cancer by up-regulating iASPP and down-regulating ASPP2.

Quantification of Helicobacter pylori in gastric mucosa by real-time polymerase chain reaction: comparison with traditional diagnostic methods

The aim of this study was to determine the main diagnostic validity parameters of a quantitative real-time polymerase chain reaction (PCR) system for detecting Helicobacter pylori in gastric biopsies. Prospective study. The real-time PCR has an internal control for eliminating the false negatives. Our system has a good diagnostic capacity compared with the gold standard and was superior in antral mucosa: area under the curve was 0.91 for antrum (95% confidence interval [CI] 0.87 to 0.96) and 0.83 for corpus (95% CI 0.77 to 0.9). The optimum cut-off point was 3.56 microorganisms/cell for antrum (sensitivity 83.5% [95% CI 74.2 to 89.9]; specificity 91.3% [95% CI 82.3 to 96.0]; positive predictive value 92.2%; negative predictive value 81.8%). The positive likelihood ratios were 9.61 and 8.52 for antrum and corpus, respectively. With the cut-off point that maximises the Youden index, 8.7% false positives were obtained. Our methodology is useful for diagnosing infection due to H. pylori and the false positives detected probably correspond to patients who were actually infected but the infection was not detected by traditional techniques. The clinical importance of these cases should be studied in greater detail since they may involve colonisations unrelated to the patient's digestive pathology.

Isolation of Helicobacter pylori in gastric mucosa and susceptibility to five antimicrobial drugs in Southern chile.

Helicobacter pylori colonizes more than 50% of the world population thus, it is considered an important cause of gastric cancer.The aim of this study was to determine the isolation frequency of H. pylori in Southern Chile from patients with symptomatology compatible with gastritis or gastric ulcer and to correlate these findings with demographic parameters of infected patients and the susceptibility profiles of the isolated strains to the antimicrobial drugs used in the eradication treatments.A total of 240 patients were enrolled in the study. Each gastric biopsy was homogenized and seeded onto blood agar plates containing a selective antibiotics mixture (DENT supplement). Plates were incubated at 37° C in a microaerophilic environment for five days.The susceptibility profiles to amoxicillin, ciprofloxacin, clarithromycin, tetracycline and metronidazole were determined using the E-test method.H. pylori was isolated from 99 patients (41.3%) with slightly higher frequency in female (42% positive cultures) than male (40.2% positive cultures).With regard to age and educational level, the highest isolation frequencies were obtained in patients between 21–30 (55%) and 41–50 (52.6%) years old, and patients with secondary (43.9%) and university (46.2%) educational levels.Nineteen (21.6%) strains showed resistance to at least one antimicrobial drug. Tetracycline was the most active antimicrobial in vitro, whereas metronidazole was the less active. One strain (5.3%) showed resistance to amoxicillin, clarithomycin and metronidazole, simultaneously.

P277 Prevalence of Helicobacter pylori in gastric mucosa and dental plaque in Sari Township population and its association with oral hygiene, Iran, 2007

P277 Prevalence of Helicobacter pylori in gastric mucosa and dental plaque in Sari Township population and its association with oral hygiene, Iran, 2007

DETECTION OF Helicobacter pylori IN GASTRIC MUCOSA OF SHEEP: PRELIMINARY RESULTS

Helicobacter pylori is an organism widespread in humans and sometimes responsible for serious illnesses. It has been hypothesized the existence of animal reservoirs, and that the infection route by H. pylori involves multiple pathways including food-borne transmission as the microorganism has been detected from sheep, goat and cow milk. This work reports the preliminary results of a survey conducted in order to investigate the presence of H. pylori in gastric mucosa of sheep slaughtered in Apulia region (Italy) employing a Nested Polymerase Chain Reaction (Nested-PCR) assay for the detection of the phosphoglucosamine mutase gene (glmM), as screening method followed by conventional bacteriological isolation. Out of the 50 gastric mucosa samples examined, 3 (6%) resulted positive for the presence of glmMgene, but at this time no strains were isolated. The results deserve further investigations to asses the role of ruminants as possible reservoirs of H. pylori.

Microbe-induced epigenetic alterations in host cells: The coming era of patho-epigenetics of microbial infections

It is well documented that the double-stranded DNA (dsDNA) genomes of certain viruses and the proviral genomes of retroviruses are regularly targeted by epigenetic regulatory mechanisms (DNA methylation, histone modifications, binding of regulatory proteins) in infected cells. In parallel, proteins encoded by viral genomes may affect the activity of a set of cellular promoters by interacting with the very same epigenetic regulatory machinery. This may result in epigenetic dysregulation and subsequent cellular dysfunctions that may manifest in or contribute to the development of pathological changes (e.g. initiation and progression of malignant neoplasms; immunodeficiency). Bacteria infecting mammals may cause diseases in a similar manner, by causing hypermethylation of key cellular promoters at CpG dinucleotides (promoter silencing, e.g. by Campylobacter rectus in the placenta or by Helicobacter pylori in gastric mucosa). I suggest that in addition to viruses and bacteria, other microparasites (protozoa) as well as macroparasites (helminths, arthropods, fungi) may induce pathological changes by epigenetic reprogramming of host cells they are interacting with. Elucidation of the epigenetic consequences of microbe-host interactions (the emerging new field of patho-epigenetics) may have important therapeutic implications because epigenetic processes can be reverted and elimination of microbes inducing patho-epigenetic changes may prevent disease development.

Effect of the flavonoid quercetin on inflammation and lipid peroxidation induced by Helicobacter pylori in gastric mucosa of guinea pig

Helicobacter pylori infection induces an inflammatory response in the gastric mucosa. Activation of polymorphonuclear leukocytes can produce oxidative damage to gastric tissue through intermediary radicals of oxygen and nitrogen. Vegetable extracts containing polyphenols of the flavonoid family have antibacterial activity, and the flavonoid quercetin possesses anti-H. pylori activity in vitro. The aim of this study was to analyze the effect of oral administration of pure quercetin on inflammation and lipid peroxidation induced by H. pylori in the gastric mucosa of the guinea pig. Sixty days after oral infection with H. pylori guinea pigs received 200 mg/kg of quercetin daily by mouth for 15 days. The infiltration index of inflammatory cells and bacterial density in both the pyloric antrum and corpus were histologically determined by myeloperoxidase histochemistry, hematoxylin-eosin, and modified Giemsa stains. The lipid hydroperoxide content was assessed by the orange xylenol spectrophotometric method. Quercetin significantly reduced the infiltration index of mononuclear cell and bacterial colonization in the pyloric antrum and corpus. In the antrum of infected quercetin-treated animals, a significant diminution of neutrophil leukocyte infiltration was observed compared with the infected nonquercetin-treated animals. In the antrum, the lipid hydroperoxide concentration was significantly decreased in infected animals treated with quercetin, whereas in the corpus no significant differences were observed. Our results indicate that in vivo oral quercetin administration decreases H. pylori infection in the gastric mucosa and reduces both the inflammatory response and lipid peroxidation.

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Helicobacter pylori is associated with gastric disorders in humans and some experimental animals, and possesses the luxS/type 2 autoinducer (AI-2) system. The effects of a specific luxS mutation on the characteristics of H. pylori were examined. On 0.3 % agar medium, motility of H. pylori HPKY08 (luxS : : cat) was significantly lower than that of wild-type H. pylori TK1402. The luxS-complemented strain HPKY21 exhibited motility comparable to that of H. pylori TK1402. It was shown that the luxS/AI-2 system plays an important role in H. pylori motility. The luxS mutant exhibited a reduced infection rate relative to the wild-type parent strain TK1402 in a Mongolian gerbil model. At 3 months after oral inoculation, lower numbers of H. pylori were detected by semi-quantitative real-time reverse transcription PCR (qRT-PCR) in luxS(-) mutant-infected gerbils than in TK1402-infected gerbils. Gastric inflammation and increased antibody titre for H. pylori were observed in TK1402-infected gerbils only.

Characterization of murine monoclonal antibodies againstHelicobacter pylorilipopolysaccharide specific for Lexand Leyblood group determinants

The cell envelope of Helicobacter pylori contains lipopolysaccharide (LPS), the O-chain of which expresses type 2 Lex and Ley blood group antigens, which mimic human gastric mucosal cell-surface glycoconjugates and may contribute to the survival of H. pylori in gastric mucosa. Here we describe the generation of monoclonal antibodies specific for Lex and Ley blood group determinants and the characterization of their binding properties using purified, structurally defined H. pylori LPS, synthetic glycoconjugates, and H. pylori cells. Analysis of oligosaccharide binding by SPR provided a rapid and reliable means for characterization of antibody affinities. One of the antibodies, anti-Lex, was of IgG3 subclass and had superior binding characteristics as compared with the commercially available anti-Lex IgM. These antibodies could have potential in the immunodiagnosis of certain types of cancer, in serotyping of H. pylori isolates, and in structure-function studies.

Oral Vaccination Against Helicobacter pylori with Recombinant Cholera Toxin B‐Subunit

The innocuous pure recombinant cholera toxin B-subunit (rCTB) is very attractive as a strong adjuvant for host immunization, but little is known about rCTB's gastric mucosal immunoadjuvanticity against Helicobacter pylori. The immunoadjuvanticity of rCTB against H. pylori was tested. Mice were immunized with sonicated H. pylori and rCTB orally or intranasally and sacrificed on day 42 after immunization. Passive cutaneous anaphylaxis (PCA) test was performed to evaluate IgE-mediated anaphylaxis with serum from mice to which H. pylori-antigen with rCTB had been administered. Immunoglobulin titer specific to H. pylori in serum, lavation of the gastrointestinal tracts and feces were examined. Gastritis in vaccinated mice after a challenge was assessed with the scoring defined from grading of gastric inflammation. H. pylori proliferation after immunization was investigated by counting colony forming units (CFU) per gram of stomach tissue. PCA test exhibited no reactions against the serum from mice immunized with H. pylori-antigen with rCTB administered orally and intranasally. Oral and nasal coadministrations of rCTB significantly raised systemic and mucosal immunities against H. pylori and suppressed proliferation of H. pylori in gastric mucosa. The score of gastritis in mice immunized orally was significantly higher than that of mice immunized nasally due to postimmunization gastritis. Only oral administration of rCTB suppressed H. pylori proliferation as compared with intranasal administration and without rCTB. The present study indicated that rCTB has systemic and mucosal immunoadjuvanticities against H. pylori and that oral vaccination with rCTB might additively support antibiotic eradication.

Long-term infection of Mongolian gerbils with Helicobacter pylori: microbiological, histopathological, and serological analyses.

The effects of long-term infection with Helicobacter pylori on the gastric mucosa of Mongolian gerbils were examined. Colonization by H. pylori was evaluated by both microaerobic cultivation and real-time reverse transcriptase PCR (RT-PCR). Persistent infection with H. pylori in gastric mucosa was detected by real-time RT-PCR during 6 months after infection, but no H. pylori was isolated 4 months after infection by cultivation. Infiltration with neutrophils and mononuclear cells was observed from 2 months after infection. Both intestinal metaplasia and gastric atrophy were also detected from 2 months after infection. The results by enzyme-linked immunosorbent assay indicated that antibody titers against whole H. pylori antigens, H. pylori heat shock protein 60 (HSP60), and Escherichia coli GroEL were significantly higher in the infected gerbils than in noninfected gerbils. After long-term infection with H. pylori for 18 months, marked atrophy of gastric mucosa and multiple cysts in the submucosa were observed in the glandular stomach of the infected gerbils. In addition, squamous cell papilloma with hyperkeratosis was observed in cardia of all the infected gerbils. These results indicate that evaluation of bacterial colonization during long-term infection can be done by real-time RT-PCR and that mucosal damage might be induced by host immune response against whole H. pylori antigen.