Lipid raft microdomains mediate class A scavenger receptor-dependent infection of Brucella abortus
Lipid raft microdomains mediate class A scavenger receptor-dependent infection of Brucella abortus
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DOI：
10.1016/j.micpath.2004.04.002
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发表时间：
2004-07-01
影响因子：
3.8
通讯作者：
Shirahata, T
中科院分区：
文献类型：
--
作者：
Kim, S;Watarai, M;Shirahata, T
流产布鲁氏菌是一种兼性细胞内细菌，可以在巨噬细胞内生存。流产布鲁氏菌的细胞内复制需要 VirB 复合物，该复合物与接合 DNA 转移系统高度相似。在这项研究中，我们发现巨噬细胞的 A 类清道夫受体 (SR-A) 是内化流产布鲁氏菌所必需的，并有助于在小鼠中建立细菌感染。 SR-A 缺陷小鼠的巨噬细胞抑制野生型菌株和 virB4 突变体的内化和细胞内复制，并且 SR-A 缺陷小鼠的细菌增殖受到抑制。将来自流产布鲁氏菌和鼠伤寒沙门氏菌的脂多糖添加到巨噬细胞中抑制细菌内化，但不添加来自大肠杆菌的脂多糖。 VirB 依赖性细菌内化诱导 SR-A 定位到耐去垢剂膜脂筏中。这些结果表明，流产布鲁氏菌通过使用SR-A作为受体内化到巨噬细胞中，并且流产布鲁氏菌的VirB IV型分泌系统调节依赖于SR-A的信号转导以形成复制性吞噬体，并且这是由脂筏介导的。 (C) 2004 Elsevier Ltd. 保留所有权利。
Brucella abortus is a facultative intracellular bacterium that can survive inside macrophages. Intracellular replication of B. abortus requires the VirB complex, which is highly similar to the conjugative DNA transfer system. In this study, we showed that a class A scavenger receptor (SR-A) of macrophages is required to internalize B. abortus and contributes to the establishment of bacterial infection in mice. Macrophages from SR-A-deficient mice inhibited internalization and intracellular replication of both wild type strain and the virB4 mutant, and that bacterial proliferation was inhibited in SR-A-deficient mice. Adding lipopolysaccharide from B. abortus and Salmonella enterica serovar Typhimurium, but not from Escherichia coli, to macrophages inhibited bacterial internalization. VirB-dependent bacterial internalization induced localization of SR-A into detergent-resistant membrane lipid rafts. These results indicate that B. abortus internalizes into macrophages by using SR-A as a receptor and that the VirB type IV secretion system of B. abortus regulates signal transduction dependent on SR-A to form replicative phagosomes, and which is mediated by lipid rafts. (C) 2004 Elsevier Ltd. All rights reserved.