Mimuro Lab／Division of Infectious Disease Department of Infection Microbiology
Bacteria-gut interplay and the host immune response are the most critical issues in determining the fate of bacterial infections and the severity of the diseases. Our group has been studying the pathogenesis of mucosal infectious bacteria, such as Helicobacter pylori, Shigella, enteropathogenic Escherichia coli, and Streptococcus pyogenes, by defining the molecular and cellular mechanisms of infections and the roles of pathogenic factors as well as the host factors in infections.
In the Mimuro laboratory, researchers are exploring the pathogenesis of mucosal infectious bacteria, including H. pylori, Shigella, enteropathogenic E. coli, and S. pyogenes.
H. pylori transports effector proteins and other molecules into host epithelial cells via a Type IV secretion system and/or outer membrane vesicles. Researchers are studying how these effectors cause diseases such as gastritis, gastric ulcers, and cancer. They are also trying to elucidate the mechanisms that enable long-term infection of H. pylori in the stomach. In addition, researchers are focusing on the molecular mechanisms in the host that protect against infectious bacteria. The expected output of their research will not only shed further light on bacterial pathogenesis, but also provide a new paradigm in microbiology, cell biology, immunity, and pathology, and strengthen the molecular basis for developing diagnostic products, vaccines, animal models, and therapeutic agents.
- Assoc. Prof.: Hitomi Mimuro
- Asst. Prof.: Ryo Kinoshita-Daitoku
- (1) Mutational diversity in mutY deficient Helicobacter pylori and its effect on adaptation to the gastric environment. Kinoshita-Daitoku R., et al. Biochem Biophys Res Commun. (2020) 525(3):806-811
(2) Group A Streptococcus establishes pharynx infection by degrading the deoxyribonucleic acid of neutrophil extracellular traps. Tanaka M., et al. Sci Rep. (2020)10(1):3251
(3) Shigella effector IpaH4.5 targets 19S regulatory particle subunit RPN13 in the 26S proteasome to dampen cytotoxic T lymphocyte activation. Otsubo R., et al. Cell Microbiol. (2019) 21(3):e12974.
(4) Epigenetic silencing of miR-210 increases the proliferation of gastric epithelium during chronic Helicobacter pylori infection. Kiga K., et al. Nat Commun. (2014) 5:4497