［総説］細菌性赤痢の病態形成における感染と宿主応答の分子機構
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概要
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Shigella are highly adapted human pathogens that cause bacillary dysentery (also referred to shigellosis). When the pathogen reaches the human colon, bacteria translocate through the epithelial barrier by way of the M Cells that overlay the solitary lymphoid nodules. Once it reaches the underlying M cells, Shigella infects the resident macrophages and induces proinflammatory cell death with interleukin-1 $ \beta $ release. Meanwhile, a bacterium release from the macrophages enters enterocytes via the basolateral surface by directing membrane ruffling and macropmocytosis, The bacterium is surrounded by a phagocytic vacuole; however, it immediately disrupts the membrane to escape into the cytoplasm, where it can multiply and move by inducing actin polymerization at one pole of the bacterium, allowing intracellular spread within the cytoplasm as well as into adjacent epithelial cells. The prominent pathogenic feature of Shigella is their ability to invade a variety of host cells, including epithelial cells, macrophages, and dendritic cells, which leads to severe inflammatory responses in intestinal tissue. Thus, the ability of Shigella spp. to infect host cells, including the continuous intra-and intercellular spreading, is essential for leading to bacillary dysentery. Recently, our molecular and cell biological approaches to the study of linkages between the bacterial factors and host cellular ligands have shed light on the molecular basis of actin polymerization and of proinflammatory responses directed by intracellular bacteria. Here, we summarize and discuss the present model for the interaction between bacteria and host cells on Shigella infection.
- 琉球医学会の論文
琉球医学会 | 論文
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