Resolution Of Gastritis Research Articles

Cholesterol glucosylation-based survival strategy in Helicobacter pylori.

Helicobacter pylori is a major chronic health problem, infecting more than half of the population worldwide. H.pylori infection is linked with various clinical complications ranging from gastritis to gastric cancer. The resolution of gastritis and peptic ulcer appears to be linked with the eradication of H. pylori. However, resistance to antibiotics and eradication failure rates are reaching alarmingly high levels. This calls for urgent action in finding alternate methods for H.pylori eradication. Here, we discuss the recently identified mechanism of H.pylori known as cholesterol glucosylation, mediated by the enzyme cholesterol-α-glucosyltransferase, encoded by the gene cgt. Cholesterol glucosylation serves several functions that include promoting immune evasion, enhancing antibiotic resistance, maintaining the native helical morphology, and supporting functions of prominent virulence factors such as CagA and VacA. Consequently, strategies aiming at inhibition of the cholesterol glucosylation process have the potential to attenuate the potency of H.pylori infection and abrogate H.pylori immune evasion capabilities. Knockout of H.pylori cgt results in unsuccessful colonization and elimination by the host immune responses. Moreover, blocking cholesterol glucosylation can reverse antibiotic susceptibility in H.pylori. In this work, we review the main roles of cholesterol glucosylation in H.pyloriand evaluate whether this mechanism can be targeted for the development of alternate methods for eradication of H.pylori infection.

Severe CMV Gastritis Associated With Pembrolizumab Therapy

Introduction: Immunotherapy with checkpoint protein inhibitors has shown effectiveness in the management of malignancy, including metastatic melanoma. However, use of these medications has been limited by gastrointestinal complications. We report a rare case of severe CMV gastritis associated with pembrolizumab immunotherapy for malignant melanoma. Case: A 72 year old male with stage 4 malignant melanoma, with metastasis to lung and brain, was receiving immunotherapy with the PD-1 inhibitor pembrolizumab. Following 8 cycles of pembrolizumab he was admitted with several weeks of persistent epigastric pain, non-bloody, non-bilious emesis, poor oral intake, and 20 lbs weight loss over one month. A PET-CT scan done prior to admission to assess response of therapy, showed multiple small soft tissue nodules around the lesser curvatures of stomach. An EGD was performed which showed severe desquamative gastritis. The entire stomach appeared edematous, erythematous, friable and erosive, which raised suspicion for immune mediated gastritis. The esophagus and duodenum appeared normal. Pathology revealed severe acute inflammation with almost complete absence of surface mucosa and dense neutrophilic infiltration of the lamina propria and crypts. IHC for CMV was positive. Patient was initially treated with steroids (equivalent to 1 mg / kg prednisone for three weeks with gradual taper), high intensity proton pump inhibitor therapy, as well as valganciclovir for CMV. The patient's symptoms improved and immunotherapy was resumed with pembrolizumab. He had follow up EGDs after 2 months and 1 year with near resolution of gastritis and clearance of CMV gastritis.2667_A Figure 1 No Caption available.2667_B Figure 2 No Caption available.2667_C Figure 3 No Caption available.Discussion: PD-1 inhibitors like nivolumab and pembrolizumab, have been commonly implicated in severe cases of enterocolitis and rarely in esophagitis and gastritis. These adverse effects are immune mediated. Rare cases of CMV activation have also been reported with PD-1 inhibitor therapy. Our case emphasizes that role of viruses like CMV should be suspected in severe cases of gastritis or colitis due to immunotherapy. In our patient immunotherapy was resumed without recurrence of GI symptoms with one year follow-up.

Response to “Eradication of Helicobacter pylori and Resolution of Gastritis in the Gastric Mucosa of IL‐10‐Deficient Mice”

HelicobacterVolume 11, Issue 2 p. 135-136 Response to “Eradication of Helicobacter pylori and Resolution of Gastritis in the Gastric Mucosa of IL-10-Deficient Mice” Kathryn A. Eaton DVM, PhD, Kathryn A. Eaton DVM, PhD Unit for Laboratory Animal Medicine, 018 Animal Research Facility, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0614, USASearch for more papers by this author Kathryn A. Eaton DVM, PhD, Kathryn A. Eaton DVM, PhD Unit for Laboratory Animal Medicine, 018 Animal Research Facility, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0614, USASearch for more papers by this author First published: 08 March 2006 https://doi.org/10.1111/j.1523-5378.2006.00389.xCitations: 3 Reprint requests to: Kathryn A. Eaton, Unit for Laboratory Animal Medicine, 018 Animal Research Facility, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0614, USA E-mail: [email protected] Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume11, Issue2April 2006Pages 135-136 RelatedInformation

Eradication of Helicobacter pylori and Resolution of Gastritis in the Gastric Mucosa of IL‐10‐Deficient Mice

Helicobacter pylori has been shown to induce pronounced gastric inflammation in the absence of interleukin-10 (IL-10) by 6 weeks post inoculation. The ability of IL-10(-/-) mice to eradicate H. pylori has not been demonstrated, possibly due to early sacrifice. Therefore, the long-term effect of enhanced gastritis on H. pylori colonization was determined in IL-10(-/-) mice. C57BL/6 and IL-10(-/-) mice were infected with H. pylori and assessed for the degree of gastritis, bacterial load, and in vitro T-cell recall response at 4 and 16 weeks of infection. Infection of IL-10(-/-) mice resulted in significantly more severe gastritis than wild-type control mice and eradication of H. pylori by 4 weeks post inoculation. By 16 weeks, the level of gastritis in IL-10(-/-) was reduced to the levels observed in wild-type mice. Splenocytes from IL-10(-/-) mice were prone to produce significantly greater amounts of IFN-gamma than wild-type mice when stimulated with bacterial antigens. These results indicate that the host is capable of spontaneously eradicating H. pylori from the gastric mucosa when inflammation is elevated beyond the chronic inflammation induced in wild-type mice, and that the gastritis dissipates following bacterial eradication. Additionally, these data provide support for a model of gastrointestinal immunity in which naturally occurring IL-10-producing regulatory T cells modulate the host response to gastrointestinal bacteria.

Cure of Helicobacter pylori infection and resolution of gastritis by adoptive transfer of splenocytes in mice.

Vaccination suppresses Helicobacter pylori colonization but does not cure infection. Furthermore, postvaccination gastritis, likely induced by enhanced host response to residual colonization, may exacerbate disease. The goal of this study was to determine if adoptive transfer of C57BL/6 splenocytes to C57BL/6scid/scid (severe combined immunodeficient [SCID]) mice cures infection without exacerbating gastritis. H. pylori-infected and uninfected C57BL/6 mice and SCID recipients of normal splenocytes were killed at intervals between 5 and 51 weeks after infection. Colonization and gastritis were quantified, humoral immune responses were determined by enzyme-linked immunosorbent assay, and cellular immune responses were determined by delayed-type hypersensitivity response and by a proliferative response of cultured splenocytes to H. pylori sonicate. In infected C57BL/6 mice, gastritis developed gradually and bacterial colonization diminished but persisted throughout the experiment. In contrast, gastritis in infected recipient SCID mice developed rapidly and bacterial colonization decreased precipitously. Gastritis in those mice peaked 9 weeks after adoptive transfer, however, and began to resolve. By 45 weeks after transfer, gastritis had returned to background levels and bacteria were no longer detectable. Resolution of gastritis and elimination of infection were associated with a cellular but not humoral immune response to H. pylori antigens. These results demonstrate that although the host response fails to clear bacterial colonization in normal mice, enhanced cellular immune responses in recipient SCID mice are capable of clearing H. pylori infection and allowing resolution of gastritis. Thus, immune mechanisms of cure exist, and effective and safe vaccination protocols may be feasible.

Cure of helicobacter pylori and resolution of gastritis by adoptive transfer of splenocytes in mice

Cure of helicobacter pylori and resolution of gastritis by adoptive transfer of splenocytes in mice

Resolution of gastritis after successful eradication of Helicobacter pylori using a triple regimen of pantoprazole, amoxicillin and clarythromycin for one week

Resolution of gastritis after successful eradication of Helicobacter pylori using a triple regimen of pantoprazole, amoxicillin and clarythromycin for one week

Helicobacter pylori and gastroduodenal disease.

Helicobacter pylori infection is now recognized as the primary cause of active chronic gastritis in humans. Most infected persons remain asymptomatic, but are at increased risk for the development of peptic ulcer disease and possibly gastric cancer. The pathogenesis of this infection is not well understood, but motility and urease activity are virulence factors in an animal model. The eradication of H. pylori infection is associated with resolution of gastritis and a decreased rate of duodenal ulcer recurrence.