Choi Chul Hee, Lee Jun Sik, Lee Yoo Chul, Park Tae In, Lee Je Chul
Department of Microbiology, Kyungpook National University School of Medicine, Daegu, Korea.
BMC Microbiol. 2008 Dec 10;8:216. doi: 10.1186/1471-2180-8-216.
Acinetobacter baumannii is a nosocomial pathogen of increasing importance, but the pathogenic mechanism of this microorganism has not been fully explored. This study investigated the potential of A. baumannii to invade epithelial cells and determined the role of A. baumannii outer membrane protein A (AbOmpA) in interactions with epithelial cells.
A. baumannii invaded epithelial cells by a zipper-like mechanism, which is associated with microfilament- and microtubule-dependent uptake mechanisms. Internalized bacteria were located in the membrane-bound vacuoles. Pretreatment of recombinant AbOmpA significantly inhibited the adherence to and invasion of A. baumannii in epithelial cells. Cell invasion of isogenic AbOmpA- mutant significantly decreased as compared with wild-type bacteria. In a murine pneumonia model, wild-type bacteria exhibited a severe lung pathology and induced a high bacterial burden in blood, whereas AbOmpA- mutant was rarely detected in blood.
A. baumannii adheres to and invades epithelial cells. AbOmpA plays a major role in the interactions with epithelial cells. These findings contribute to the understanding of A. baumannii pathogenesis in the early stage of bacterial infection.
鲍曼不动杆菌是一种日益重要的医院病原体，但其致病机制尚未完全阐明。本研究调查了鲍曼不动杆菌侵袭上皮细胞的可能性，并确定了鲍曼不动杆菌外膜蛋白A（AbOmpA）在上皮细胞相互作用中的作用。
鲍曼不动杆菌通过拉链样机制侵袭上皮细胞，这与微丝和微管依赖性摄取机制有关。内化的细菌位于膜结合的液泡中。重组AbOmpA预处理显著抑制了鲍曼不动杆菌在上皮细胞中的黏附和侵袭。与野生型细菌相比，同基因AbOmpA突变体的细胞侵袭显著降低。在小鼠肺炎模型中，野生型细菌表现出严重的肺部病理变化，并在血液中诱导出高细菌载量，而在血液中很少检测到AbOmpA突变体。
鲍曼不动杆菌黏附并侵袭上皮细胞。AbOmpA在上皮细胞相互作用中起主要作用。这些发现有助于理解鲍曼不动杆菌在细菌感染早期的发病机制。
