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Helicobacter
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Tetsuya Tsukamoto, Yuka Kiriyama, Masae Tatematsu
Various experimental animal models have been attempted to help clarify the role of H. pylori. Lee et al.43 isolated Helicobacter felis (H. felis) from cat stomach and inoculated it in germ-free mice, resulting in colonization of the glandular stomach and induction of acute and chronic inflammation. A type of H. pylori, designated Sydney strain (SS1), established by screening of fresh clinical isolates, showed high colonizing ability and is currently widely used for mice experiments.44 The Mongolian gerbil (Meriones unguiculatus) model was successfully established to mimic human H. pylori infection, resulting in chronic active gastritis, peptic ulcers, and intestinal metaplasia resembling human lesions.45
Gastrointestinal Tract
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Judit E. Markovits, Graham R. Betton, Donald N. McMartin, Theresa Boulineau
The lamina propria of the gastric mucosa and the submucosa of control animals contain a moderate degree of inflammatory cell infiltration. In rodents, this can have a significant eosinophil content. In dogs and nonhuman primates, inflammatory infiltrates are primarily composed of mononuclear cells. In the cardiac and antral regions, these may be slight to moderate in severity, and lymphoid follicles with active germinal centers may be present, indicative of enzootic bacterial infection, for example, Helicobacter spp. (Figure 11.14a,b). A number of Helicobacter spp, including Helicobacter felis, H. bizzozeroni, and H. salomonsis are not considered pathogenic and may colonize clinically normal dogs (Baele et al. 2004; Jalava et al. 1998; Van den Bulck et al. 2005) unlike H. pylori, the main human pathogen. Dogs experimentally infected with H. pylori show gastritis, erosions, and lymphoid follicle formation (Rossi et al. 1999). The microbiological status of treated versus control dogs can be assessed using special stains on tissue, polymerase chain reaction (PCR), or Helicobacter [13C] urea breath tests (Cornetta et al. 1998). H. pylori also induces gastritis, intestinal metaplasia, and ulcer formation in Mongolian gerbils (Ikeno et al. 1999). Experimental infection of pigs with H. pylori produces a lymphocytic gastritis (Poutahidis et al. 2001), similar to the human disease. The inflammation and cell death caused by Helicobacter are believed to be caused by oxygen-free radical formation leading to adenocarcinoma in a subset of humans (Konturek et al. 2006).
Role of vacuolating cytotoxin A in Helicobacter pylori infection and its impact on gastric pathogenesis
Published in Expert Review of Anti-infective Therapy, 2020
Shamshul Ansari, Yoshio Yamaoka
Despite the possibilities of several factors, the differences in intake of particular foods, co-existence of other infection, or gut microbiota composition have been speculated to differ the gastric cancer rates between African countries and other parts of the world [133]. A study on co-infection of mice with the Heligosomoides polygyrus which is an extracellular mouse parasite and Helicobacter felis has found an alteration in the immune response to a greater extent with down-regulation of Th1 dependent IgG2a serum antibody when compared with the Th2 dependent IgG1 response leading to a reduced H. pylori mediated gastric atrophy suggesting a role of other common infections in Africa that might affect the outcome of the H. pylori infection [134].
Helicobacter pylori antibiotic eradication coupled with a chemically defined diet in INS-GAS mice triggers dysbiosis and vitamin K deficiency resulting in gastric hemorrhage
Published in Gut Microbes, 2020
Lisa Quinn, Alexander Sheh, Jessie L Ellis, Donald E Smith, Sarah L Booth, Xueyan Fu, Sureshkumar Muthupalani, Zhongming Ge, Dylan A Puglisi, Timothy C Wang, Tamas A Gonda, Hilda Holcombe, James G Fox
Our previous study demonstrates that markedly reducing enteric bacteria alone is not sufficient to cause anemia in INS-GAS when provided sufficient dietary vitamin K in a standard rodent diet (1.9 mg MD/kg of diet).17 Upon evaluating current nutritional guidelines for mice, we determined the AAD diet containing menadione (MD) at 0.5 mg/kg diet provided suboptimal levels of vitamin K.27,37 However, diet alone does not explain the hemorrhage observed as no clinically apparent anemias were observed prior to antibiotic treatment, and our previous study using INS-GAS mice on the AAD diets with 0.5 mg MD/kg of diet did not result in anemia.18 Interestingly, in the current study, two H.pylori infected mice fed increased folate (8 mg/kg diet) with no antibiotic treatment developed fatal gastric hemorrhages. While both studies used INS-GAS mice fed identical AAD diets, the studies differed in the species of gastric Helicobacter used and the location of the vivarium. The INS-GAS model has been successfully reproduced in multiple research institutions using both Helicobacter felis and H. pylori, but the severity of the disease can vary between organisms and institutions.18,38–40 Increased ulceration could exacerbate pathologies related to hypovitaminosis K and anemia. Another important variable is that the Gonda study was performed at Columbia Medical Center, while our current study was performed at MIT. Location can strongly influence the microbiome of mice, and we have previously demonstrated that alterations in the microbiota at different institutions or from different vendors can affect the pathogenesis of Helicobacter-mediated models.41,42 We have also determined that the gastric microbiome of INS-GAS mice from different institutions can change significantly and have an effect on the severity of H. pylori-induced disease (Sheh et al., unpublished data). In addition to altering Helicobacter-mediated inflammation, the changes in bacterial communities may directly alter the MKn levels in the mice in both vivariums. Further research is necessary to determine the role of different gastric Helicobacter species and the underlying microbiome in the coagulopathy described in the current study.