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Epidemiology
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Grant Theron, Ted Cohen, Christopher Dye
Besides the link between TB and asthma, interactions between other infections have come under investigation. Vigorous Th2 responses are seen in protective immune reactions to helminth infections, and helminths could modulate atopic disease while compromising the immune response to bacille Calmette-Guerin (BCG) and M. tuberculosis.158–160 Another common organism Helicobacter pylori, estimated to infect over 4 billion people, may play a role in TB: H. pylori-infected macaques challenged with low doses of M. tuberculosis are less likely to progress to active TB compared to H. pylori-uninfected macaques and, in humans, latently infected household contacts who did not develop active TB within two years were more likely to be infected with H. pylori than contacts that go on to develop active disease.161 Conversely, mice with Helicobacter hepaticus (a human pathogen) gut infection have subclinical inflammation, and drastic impairment of immune control of the growth of subsequently administered M. tuberculosis, which results in severe lung tissue pathology.162
Commensal microbiota and its relationship to homeostasis and disease
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jonathan Braun, Elaine Y. Hsiao, Nicholas Powell
Host responses to pathogen-associated intestinal inflammation are also influenced by the microbiota. For example, Helicobacter hepaticus infection induces colitis and liver inflammation in conventionally colonized animals. However, germ-free mice monoassociated with H. hepaticus do not develop disease, implying that components of the conventional microbiota are not necessarily innocent bystanders in the company of pathogens. Interestingly, patients with IBD have detectable circulating antibodies and T-cell specificities directed against normal constituents of their intestinal microbiota.
Translocation of Helicobacter hepaticus synergizes with myeloid-derived suppressor cells and contributes to breast carcinogenesis
Published in OncoImmunology, 2022
Huan Deng, Sureshkumar Muthupalani, Susan Erdman, Haibo Liu, Zhengchuan Niu, Timothy C. Wang, James G. Fox
Helicobacter hepaticus (H. hepaticus) is a bacterium that has been found in the liver and intestine of inbred mice.8 Accumulating evidence indicates its important role in promoting typhlitis and colitis, raising the possibility that H. hepaticus and related species may contribute to intestinal dysbiosis. The use of H. hepaticus infection in diverse mouse models, including IL10−/− and Rag−/−, has revealed that the innate immune system plays a critical role in the development of colitis and colitis-associated cancer.9,10H. hepaticus infection has also been demonstrated to trigger precancerous lesion of colon in ApcMin/+ mice.10–12 Of particular note is the fact that H. hepaticus-induced microbial dysbiosis can promote the development of mammary and prostate tumors in Rag−/−; ApcMin/+ murine model, presumably through modulation of innate immunity.11,13–16 A recent study has supported this view, as it was shown that alterations in intestinal microbiota are also involved in the development of malignant brain tumor.17
The role of the microbiome in drug resistance in gastrointestinal cancers
Published in Expert Review of Anticancer Therapy, 2021
Ingrid Garajová, Rita Balsano, Heling Wang, Francesco Leonardi, Elisa Giovannetti, Dongmei Deng, Godefridus J. Peters
Hepatobiliary and pancreatic cancers are aggressive diseases with a poor prognosis [41–44]. Though pancreas, gallbladder, and liver are not part of the alimentary canal, these organs are essential to digestion and pancreatic cancer, biliary tract, and liver cancer are exposed to the gut microbiome via blood flow through the portal vein [45]. It has been demonstrated that the composition of intestinal microbiota is associated with the progression of nonalcoholic steatohepatitis [46] and liver cirrhosis [47] which are correlated with liver tumor development. Furthermore, a possible role of H. pylori and other Helicobacter species has been found in hepatocellular cancer. In particular, Helicobacter hepaticus may colonize the bile tract and the large intestine and promote liver tumor development in a mouse model [48]. Similarly, biliary tract cancers have been associated with Helicobacter species, in particular H. pylori, Helicobacter bilis and H. hepatics [49,50]. In addition, Salmonella typhi infection is associated with an increased risk of gallbladder cancer [51].
Pathobionts: mechanisms of survival, expansion, and interaction with host with a focus on Clostridioides difficile
Published in Gut Microbes, 2021
Harish Chandra, Krishna Kant Sharma, Olli H. Tuovinen, Xingmin Sun, Pratyoosh Shukla
The GI tract harbors predominantly members of the Firmicutes, Bacteroidetes, and Actinobacteria phyla.5 The human microbiome contributes about 100-fold more genes over the human genome that empower the host with enzymes for metabolism and energy needs such as biosynthesis of vitamins, digestion of polysaccharides, and degradation of mucus.6 The microbiome helps maintain integrity of the epithelial barrier and prevent pathogen colonization.7 The interactions of the components of the microbiota with the mucosal immune system are highly dynamic and is critical for the maintenance of the epithelial barrier and the sensitization of the mucosal innate immune cells for developing immune tolerance against the components of the microbiota.8 However, repeated exposure of certain groups of microbes in the microbiota, known as pathobionts, may result in damage to the host epithelial barrier by inducing exacerbated innate inflammatory response via activation of pro-inflammatory cytokines, inflammasome, induction of specific TH17 T cells, and recruitment of neutrophils to the site of infections.9 These microbes become pathobionts under certain conditions of endogenous and exogenous factors that alter the gut microbiota contributions to the pathological conditions in the gut. For example, Helicobacter hepaticus, a component of murine gut, is implicated in large bowl disease in immunocompromised mice, while the disease is not manifested in healthy mice.10