The crosstalk between microbiome and immune response in gastric cancer
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MDPI AG
Abstract
Gastric cancer is the end result of a complex interplay between host genetics, environmental factors, and microbial factors. The link between gut microbiome and gastric cancer has been attributed to persistent activation of the host’s immune system by gut microbiota. The end result of this dysregulated interaction between host epithelium and microbes is a state of chronic inflammation. Gut bacteria can promote anti-tumor immune responses through several mechanisms. These include triggering T-cell responses to bacterial antigens that can cross-react with tumor antigens or cause tumor-specific antigen recognition; engagement of pattern recognition receptors that mediate pro-immune or anti-inflammatory effects or via small metabolites that mediate systemic effects on the host. Here we review the role of the gut microbiome including H. pylori and non-H. pylori gastric bacteria, the immune response, and immunotherapy using checkpoint inhibitors. We also review the evidence for cross talk between the gut microbiome and immune response in gastric cancer. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
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Keywords
Ctla-4, Gastric cancer, Gut microbiome, H. pylori, Immune checkpoint inhibitors, Immune response, Immunotherapy, Lactic acid bacteria, Pd-l1, Adenocarcinoma, Gastric mucosa, Gastrointestinal microbiome, Humans, Stomach neoplasms, Chloroplast dna, Cytotoxic t lymphocyte antigen 4 antibody, Immunological antineoplastic agent, Programmed death 1 ligand 1, Tumor marker, Actinobacteria, Bacterium, Bacteroidetes, Cancer immunotherapy, Cross reaction, Epstein barr virus, Firmicutes, Fusobacteria, Helicobacter pylori, High throughput sequencing, Human, Intestine flora, Microsatellite instability, Proteobacteria, Review, Stomach cancer, Stomach carcinogenesis, Tumor associated leukocyte, Tumor growth, Tumor mutational burden, Tumor volume, Whole exome sequencing, Immunology, Microbiology, Stomach mucosa, Stomach tumor