小鼠树突状细胞摄取支气管败血博德特氏菌所涉及的机制。
Mechanisms involved in uptake of Bordetella bronchiseptica by mouse dendritic cells.
作者信息
Guzman C A, Rohde M, Timmis K N
机构信息
Division of Microbiology, GBF-National Research Centre for Biotechnology, Braunschweig, Germany.
出版信息
Infect Immun. 1994 Dec;62(12):5538-44. doi: 10.1128/iai.62.12.5538-5544.1994.
Abstract
The invasion and intracellular survival of Bordetella bronchiseptica in mouse dendritic cells were investigated. The results obtained suggest that B. bronchiseptica binds specifically to glycosylated receptors present on the plasma membrane of dendritic cells, thereby inducing a signal that triggers an actin polymerization-dependent phagocytic process, probably via a protein kinase-dependent transducing phosphorylation signal. The energy required for the uptake process by host cells is provided mainly by the glycolytic pathway. An intact microtubule system and de novo protein synthesis in eukaryotic and prokaryotic cells are essential for efficient uptake and intracellular survival. The interaction of B. bronchiseptica with dendritic cells may be pertinent to natural infections that follow a chronic clinical course and predispose to secondary infections, and to the T-cell response involved in protective immunity following infections caused by Bordetella spp.
摘要
研究了支气管败血波氏杆菌在小鼠树突状细胞中的侵袭和细胞内存活情况。所得结果表明，支气管败血波氏杆菌特异性结合树突状细胞质膜上存在的糖基化受体，从而诱导一个信号，该信号触发一个可能通过蛋白激酶依赖性转导磷酸化信号的肌动蛋白聚合依赖性吞噬过程。宿主细胞摄取过程所需的能量主要由糖酵解途径提供。真核细胞和原核细胞中完整的微管系统和从头蛋白质合成对于有效摄取和细胞内存活至关重要。支气管败血波氏杆菌与树突状细胞的相互作用可能与遵循慢性临床病程并易引发继发性感染的自然感染以及博德特氏菌属引起的感染后参与保护性免疫的T细胞反应有关。
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