Many Gram-negative bacteria possess the type III secretion system (T3SS), which is referred to as the needle complex. The needle structure of this complex protrudes from the bacterial outer membrane, and bacterial proteins are delivered into the host when the needle structure interacts with the host plasma membrane. Any bacterial protein that perturbs the physiology of the host by translocation into host cells via T3SS is generally called an “effector”. The effector has an important role in the bacterial disease process. Recent research has demonstrated that the long-term settlement of the Bordetella species including B. pertussis is dependent on T3SS, but its mechanism has remained unclear. At our laboratory, we have clarified that BopN, which is translocated into the host via T3SS, induces the production of the anti-inflammatory cytokine IL-10, and that BopC is an effector that causes cell death. Thus, the mechanism of avoiding host immune responses using effectors has been gradually disclosed. Our laboratory has elucidated the infective strategy of Bordetella bacteria on the molecular level and is utilizing this information for the development of vaccines.
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Laboratory of Bacterial Infection
