S-Space College of Medicine/School of Medicine (의과대학/대학원) Microbiology (미생물학전공) Journal Papers (저널논문_미생물학전공)
Exploitation of the endocytic pathway by Orientia tsutsugamushi in nonprofessional phagocytes
- Chu, Hyuk; Lee, Jung-Hee; Han, Seung-Hoon; Kim, Se-Yoon; Cho, Nam-Hyuk; Kim, Ik-Sang; Choi, Myung-Sik
- Issue Date
- American Society for Microbiology
- Infect Immun. 2006 Jul;74(7):4246-53.
- Animals; Cell Line; Cell Line, Transformed; Clathrin/physiology; Endocytosis/*physiology; Endothelium, Vascular/cytology/microbiology; Fibroblasts/microbiology; Humans; Macrophages/*microbiology; Mice; Orientia tsutsugamushi/*physiology; Signal Transduction/*physiology
- Orientia tsutsugamushi, a causative agent of scrub typhus, is an obligate intracellular bacterium that requires the exploitation of the endocytic pathway in the host cell. We observed the localization of O. tsutsugamushi with clathrin or adaptor protein 2 within 30 min after the infection of nonprofessional phagocytes. We have further confirmed that the infectivity of O. tsutsugamushi is significantly reduced by drugs that block clathrin-mediated endocytosis but not by filipin III, an inhibitor that blocks caveola-mediated endocytosis. In the present study, with a confocal microscope, O. tsutsugamushi was sequentially colocalized with the early and late endosomal markers EEA1 and LAMP2, respectively, within 1 h after infection. The colocalization of O. tsutsugamushi organisms with EEA1 and LAMP2 gradually disappeared until 2 h postinfection, and then free O. tsutsugamushi organisms were found in the cytoplasm. When the acidification of endocytic vesicles was blocked by treating the cells with NH(4)Cl or bafilomycin A, the escape of O. tsutsugamushi organisms from the endocytic pathway was severely impaired, and the infectivity of O. tsutsugamushi was drastically reduced. To our knowledge, this is the first report that the invasion of O. tsutsugamushi is dependent on the clathrin-dependent endocytic pathway and the acidification process of the endocytic vesicles in nonprofessional phagocytes.
- 0019-9567 (Print)
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