scholarly journals Induction of Follicular Gastritis following Postthymectomy Autoimmune Gastritis in Helicobacter pylori-Infected BALB/c Mice

2000 ◽  
Vol 68 (1) ◽  
pp. 100-106 ◽  
Author(s):  
Chikashi Oshima ◽  
Kazuichi Okazaki ◽  
Yumi Matsushima ◽  
Mitsutaka Sawada ◽  
Tsutomu Chiba ◽  
...  

ABSTRACT Helicobacter pylori is the major causative agent of chronic antral gastritis and is thought to be involved in the pathogenesis of mucosa-associated lymphoid tissue lymphoma (MALToma) developing in the human stomach. The aim of this study was to clarify whether corporal autoimmune gastritis (AIG), which is known to decrease acidity due to destruction of parietal cells, predisposes mice toH. pylori infection, thereby leading to MALToma-like pathology. BALB/c mice in which AIG had been induced by thymectomy 3 days after birth (AIG mice) were used. The AIG mice were orally administered mouse-adapted H. pylori at the age of 6 weeks and were examined histologically and serologically after 2 to 12 months. The results were compared with those obtained from uninfected AIG mice and infected normal mice. Germinal centers were induced in the corpus in 57% of the H. pylori-infected AIG mice, which elicited anti-H. pylori antibody responses in association with upregulation of interleukin-4 (IL-4) mRNA. In these mice, parietal cells remained in the corpus mucosa. These findings were in contrast to those with the uninfected AIG mice: fundic gland atrophy due to disappearance of parietal cells associated with upregulation of gamma interferon, but not IL-4, mRNA and no germinal center formation in the corpus. These observations suggest that AIG alters the infectivity ofH. pylori, leading to MALToma-like follicular gastritis, at an early stage after H. pylori infection.

2013 ◽  
Vol 4 (4) ◽  
pp. 44-47
Author(s):  
Aleksandr Alekseyevich Zvyagin

The results of inspection of 70 children for autoimmune gastritis are represented. Children with blood serum antibodies to stomach parietal cells were selected for more profound investigation. It was shown, that autoimmune gastritis in the childhood is one of the components of multiorgan autoimmune pathology in 0-33 % of patients and is characterized by minimum clinical, morphological and endoscopic data, combination with Helicobacter pylori.


2001 ◽  
Vol 69 (3) ◽  
pp. 1714-1721 ◽  
Author(s):  
Bernadette Lucas ◽  
Dirk Bumann ◽  
Anna Walduck ◽  
Jan Koesling ◽  
Leyla Develioglu ◽  
...  

ABSTRACT Protection in the murine model of Helicobacter pyloriinfection may be mediated by CD4+ T cells, but the mechanism remains unclear. To better understand how protection occurs in this model, we generated and characterized H. pyloriurease-specific CD4+ T cells from BALB/c mice immunized with Salmonella enterica serovar Typhimurium expressingH. pylori urease (subunits A and B). The CD4+ T cells were found to be specific for subunit A (UreA). Upon antigen-specific stimulation, expression of interleukin 4 (IL-4), IL-10, gamma interferon (IFN-γ), and tumor necrosis factor alpha was induced. Immunocytochemical analysis showed that the majority of cells produced IFN-γ and IL-10. Adoptive transfer of the UreA-specific CD4+ T cells into naive syngeneic recipients led to a threefold reduction in the number of bacteria in the recipient group when compared to that in the nonrecipient group. Stomach colonization was also reduced significantly after transfer of these cells into patently infected mice. Adoptive transfer of UreA-specific CD4+ T cells into IL-4 receptor α chain-deficient BALB/c mice indicated that IL-4 and IL-13 were not critical in the control of bacterial load. In addition, synthetic peptides were used to identify three functional T-cell epitopes present in subunit A which were recognized by the UreA-specific T cells. Analysis of H. pylori-specific cellular immune responses in recipient challenged and nonrecipient infected mice indicated a strong local restriction of the response in infected animals. The implications of these findings for the mechanism of protection and the development of peptide-based vaccination are discussed.


1998 ◽  
Vol 5 (3) ◽  
pp. 288-293 ◽  
Author(s):  
A. Mattsson ◽  
A. Tinnert ◽  
A. Hamlet ◽  
H. Lönroth ◽  
I. Bölin ◽  
...  

ABSTRACT In this study we have determined systemic and local antibody responses against different Helicobacter pylori antigens inH. pylori-infected and noninfected subjects. In addition, we studied whether differences in antibody responses between patients with duodenal ulcers and asymptomatic H. pylori carriers might explain the different outcomes of infection. Sera and in most instances gastric aspirates were collected from 19 duodenal ulcer patients, 15 asymptomatic H. pylori carriers, and 20 noninfected subjects and assayed for specific antibodies against different H. pylori antigens, i.e., whole membrane proteins (MP), lipopolysaccharides, flagellin, urease, the neuraminyllactose binding hemagglutinin HpaA, and a 26-kDa protein, by enzyme-linked immunosorbent assay. The H. pylori-infected subjects had significantly higher antibody titers against MP, flagellin, and urease in both sera and gastric aspirates compared with the noninfected subjects. Furthermore, the antibody titers against HpaA were significantly elevated in sera but not in gastric aspirates from the infected subjects. However, no differences in antibody titers against any of the tested antigens could be detected between the duodenal ulcer patients and the asymptomatic H. pyloricarriers, either in sera or in gastric aspirates.


2016 ◽  
Vol 6 (11) ◽  
pp. 942-946
Author(s):  
Shiva Raj K.C. ◽  
A Lakhey ◽  
K Koirala ◽  
GL Amatya

Background: Dyspepsia is a prevalent complaint in general practice and gastrointestinal clinics. Helicobacter pylori have major causal relationship with gastro duodenal disease. The following study seeks to identify the prevalence of H. pylori based on histology and to correlate endoscopic findings with histopathology.Materials and Methods: This was a cross-sectional observational study conducted in GRP Polyclinic and Om Hospital and research centre from April 2015-September 2015. The upper gastrointestinal endoscopic findings were recorded and were correlated with histopathological findings. All the relevant data were collected and analysed using Statistical Package of Social Sciences version 16 for windows.  Results: Endoscopy finding was divided into reflux esophagitis, antral gastritis, duodenitis, duodenal ulcer, gastric ulcer, and gastric cancer. Duodenal ulcer and gastric ulcer was noted more frequently in males than in females (55.0% vs. 45.0% and 58.2% vs. 41.8%), respectively, P < 0.001).Chronic follicular gastritis was the most common in gastric ulcer (41.7%), whereas chronic persistent gastritis was common in non-ulcerative disease. Chronic active gastritis and chronic follicular gastritis were more common in ulcerative diseases, whereas chronic persistent gastritis was more common in gastritis and duodenitis (P < 0.001). The overall prevalence of H. pylori infection was 68.1% with male preponderance. Chronic active gastritis had highest prevalence of H. pylori (84.8%), followed by chronic follicular gastritis (84.1%) and chronic persistent gastritis (p value < 0.001.Conclusion: Rate of H. pylori infected patients with dyspepsia was high. Ulcerative lesions were more common in males than in females with higher rate of infection with H. Pylori.  Histological diagnosis of chronic active gastritis and chronic follicular gastritis was the most common pathologies in ulcerative lesions. 


2001 ◽  
Vol 69 (1) ◽  
pp. 556-558 ◽  
Author(s):  
Toni Aebischer ◽  
Stephanie Laforsch ◽  
Robert Hurwitz ◽  
Frank Brombacher ◽  
Thomas F. Meyer

ABSTRACT Vaccination of interleukin-4 (IL-4) receptor α (IL-4Rα) chain-deficient BALB/c mice with Helicobacter pylori urease and cholera toxin or with urease-expressing, live attenuatedSalmonella enterica serovar Typhimurium cells revealed that protection against H. pylori infection is independent of IL-4- or IL-13-mediated signals. A comparison of male and female mice suggests a sexual dimorphism in the extent of bacterial colonization that is particularly evident in the absence of the IL-4Rα chain.


2001 ◽  
Vol 19 (22) ◽  
pp. 4245-4251 ◽  
Author(s):  
Li-Tzong Chen ◽  
Jaw-Town Lin ◽  
Rong-Yaun Shyu ◽  
Chang-Ming Jan ◽  
Chi-Long Chen ◽  
...  

PURPOSE: High-grade mucosa-associated lymphoid tissue (MALT) lymphomas of the stomach are generally believed to be Helicobacter pylori–independent, autonomously growing tumors. However, anecdotal cases of regression of high-grade lymphomas after the cure of H pylori infection had been described. The present prospective study was conducted to evaluate the effect of anti–H pylori therapy in stage IE high-grade gastric MALT lymphomas. PATIENTS AND METHODS: Sixteen patients with H pylori infection and stage IE gastric high-grade MALT lymphoma consented to a brief antibiotic therapy as first-line treatment from June 1995 through April 2000. Then, patients underwent intensive endoscopic follow-up examinations (± endoscopic ultrasonography) with biopsy to evaluate tumor response. Patients with significant improvement of gross lesions that accompanied regression of large cells were followed up without additional treatment. Patients without significant improvement were immediately referred to systemic chemotherapy. RESULTS: Eradication of H pylori was achieved in 15 patients and was accompanied by rapid gross tumor regression and disappearance of large cells in 10. All 10 of these patients with early response had subsequent complete histologic remission of lymphoma. The complete remission rate was 62.5% (95% confidence interval, 35.8% to 89.1%). The response rate was not affected by the tumor grading (proportion of large blast cells within the tumor) but was adversely affected by the depth of tumor invasion. At a median follow-up of 43.5 months (range, 21.1 to 67.4 months), all 10 of these patients remained lymphoma-free. The median duration of complete response was 31.2 months (range, 14.4 to 49.1 months). CONCLUSION: These results suggest that high-grade transformation is not necessarily associated with the loss of H pyloridependence in early-stage MALT lymphomas of the stomach.


2002 ◽  
Vol 70 (9) ◽  
pp. 5096-5106 ◽  
Author(s):  
Patricia Londoño-Arcila ◽  
Donna Freeman ◽  
Harry Kleanthous ◽  
Aisling M. O'Dowd ◽  
Susan Lewis ◽  
...  

ABSTRACT Recombinant vaccine strains of Salmonella enterica serovar Typhi capable of expressing Helicobacter pylori urease were generated by transforming strains CVD908 and CVD908-htrA with a plasmid harboring the ureAB genes under the control of an in vivo-inducible promoter. The plasmid did not interfere with the ability of either strain to replicate and persist in human monocytic cells or with their transient colonization of mouse lungs. When administered to mice intranasally, both recombinant strains elicited antiurease immune responses skewed towards a Th1 phenotype. Vaccinated mice exhibited strong immunoglobulin G2a (IgG2a)-biased antiurease antibody responses as well as splenocyte populations capable of proliferation and gamma interferon (IFNγ) secretion in response to urease stimulation. Boosting of mice with subcutaneous injection of urease plus alum enhanced immune responses and led them to a more balanced Th1/Th2 phenotype. Following parenteral boost, IgG1 and IgG2a antiurease antibody titers were raised significantly, and strong urease-specific splenocyte proliferative responses, accompanied by IFNγ as well as interleukin-4 (IL-4), IL-5, and IL-10 secretion, were detected. Neither immunization with urease-expressing S. enterica serovar Typhi alone nor immunization with urease plus alum alone conferred protection against challenge with a mouse-adapted strain of H. pylori; however, a vaccination protocol combining both immunization regimens was protective. This is the first report of effective vaccination against H. pylori with a combined mucosal prime-parenteral boost regimen in which serovar Typhi vaccine strains are used as antigen carriers. The significance of these findings with regard to development of a human vaccine against H. pylori and modulation of immune responses by heterologous prime-boost immunization regimens is discussed.


2003 ◽  
Vol 71 (2) ◽  
pp. 794-800 ◽  
Author(s):  
Klaus Panthel ◽  
Gerhard Faller ◽  
Rainer Haas

ABSTRACT The gram-negative bacterial pathogen Helicobacter pylori is a major cause of peptic ulcer disease and a risk factor for gastric cancer in humans. Adapted H. pylori strains, such as strain SS1, are able to infect mice and are a useful model for gastric colonization and vaccination studies. In this study we used a streptomycin-resistant derivative of H. pylori SS1 to analyze the colonization behavior and the success of vaccination in wild-type (wt) and various knockout mice of the BALB/c and C57BL/6J genetic backgrounds. We here report that BALB/c interleukin-4 knockout (IL-4−/−) mice are weakly overcolonized compared to the wt strain but that the IL-12−/− knockout results in a strong overcolonization (500%). Unexpectedly, in the C57BL/6J background the same knockouts behaved in diametrically opposed manners. The IL-4−/− mutation caused a 50% reduction and the IL-12−/− knockout caused a 95% reduction compared to the wt colonization rate. For C57BL/6J mice we further analyzed the IL-18−/− and Toll-like receptor 2 knockout mutations, which showed reductions to 66 and 57%, respectively, whereas mice with the IL-10−/− phenotype were hardly infected at all (5%). In contrast, the tumor necrosis factor receptor knockout (p55−/− and p55/75−/−) mice showed an overcolonization compared to the C57BL/6J wt strain. With exception of the low-level infected C57BL/6J IL-10−/− and IL-12−/− knockout mice, all knockout mutants were accessible to a prophylactic vaccination and their vaccination behavior was comparable to that of the wt strains.


2021 ◽  
Vol 09 (01) ◽  
pp. E22-E30
Author(s):  
Minoru Kato ◽  
Noriya Uedo ◽  
Ervin Toth ◽  
Satoki Shichijo ◽  
Akira Maekawa ◽  
...  

Abstract Background and study aims The aim of this study was to elucidate the differences in image-enhanced endoscopy (IEE) findings between Helicobacter-pylori-associated and autoimmune gastritis. Patients and methods Seven H. pylori-naïve, 21 patients with H. pylori-associated gastritis and seven with autoimmune gastritis were enrolled. Mucosal atrophy in the corpus was evaluated using autofluorescence imaging and classified into small, medium and large. In a 2 × 2-cm area of the lesser curvature of the lower corpus, micromucosal pattern was evaluated by magnifying narrow band imaging and proportion of foveola (FV)- and groove (GR)-type mucosa was classified into FV > 80 %, FV 50 % to 80 %, GR 50 % to 80 %, and GR > 80 %, then a biopsy specimen was taken. Results Fifteen of 21 (71 %) H. pylori-associated gastritis patients exhibited medium-to-large atrophic mucosa at the corpus lesser curvature. All autoimmune gastritis patients had large atrophic mucosa throughout the corpus (P < 0.001). All H. pylori-naïve patients had the FV > 80 % micromucosal pattern. Nineteen of 21 (90 %) H. pylori-associated gastritis patients had varying proportions of GR- and FV-type mucosae and five of seven (71 %) autoimmune gastritis patients showed FV > 80 % mucosa (P < 0.001). Compared with patients who were H. pylori-naïve, patients with H. pylori-associated and autoimmune gastritis exhibited a higher grade of atrophy (P < 0.001), but only patients with H. pylori-associated gastritis showed a higher grade of intestinal metaplasia (P = 0.022). Large mucosal atrophy with FV > 80 % micromucosal pattern had sensitivity of 71 % (95 % CI: 29 %–96 %) and specificity of 100 % (95 % CI: 88 % to 100 %) for diagnosis of autoimmune gastritis. Conclusions IEE findings of the gastric corpus differed between H. pylori-associated and autoimmune gastritis, suggesting different pathogenesis of the two diseases.


2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Lei Feng ◽  
Changqing Deng ◽  
Yanxia Li

Objective. This study aimed to explore the associations between carotid intima-media thickness (CIMT) and early-stage diabetic kidney disease (DKD) coupled with Helicobacter pylori (H. pylori) infection in type 2 diabetic patients. Methods. A cross-sectional study including 180 type 2 diabetic participants was conducted to explore the associations between CIMT and early-stage DKD coupled with H. pylori infection, and a stepwise multivariate regression analysis evaluated the correlations of CIMT with clinical and serologic parameters. Results. The type 2 diabetic patients with early-stage DKD coupled with H. pylori infections had the highest CIMT values. Apolipoprotein B (ApoB), urine albumin/creatinine ratio (UACR), and interleukin-6 (IL-6) were independent predictors of CIMT. Conclusions. Early-stage DKD coupled with H. pylori infection may synergistically lead to significant CIMT thickening in type 2 diabetic patients. Additionally, ApoB, UACR, and IL-6 levels were important independent risk factors for increased CIMT.


Sign in / Sign up

Export Citation Format

Share Document