Membrane-associated proteins of a lipopolysaccharide-deficient mutant of Neisseria meningitidis activate the inflammatory response through toll-like receptor 2
Membrane-associated proteins of a lipopolysaccharide-deficient mutant of Neisseria meningitidis activate the inflammatory response through toll-like receptor 2
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DOI：
10.1128/iai.69.4.2230-2236.2001
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发表时间：
2001-04-01
影响因子：
3.1
通讯作者：
Golenbock, DT
中科院分区：
文献类型：
--
作者：
Ingalls, RR;Lien, E;Golenbock, DT
最近分离的脂多糖（LPS）缺陷型脑膜炎奈瑟氏球菌的突变体，使我们能够探索其他革兰氏阴性细胞壁成分在宿主对感染的反应中的作用。本研究中的实验旨在检查该突变株激活细胞的能力。虽然它明显不如亲本菌株有效，但我们发现LPS缺陷型突变体能够诱导单核细胞中的炎症反应，诱导类似于金黄色葡萄球菌的反应。LPS突变体的细胞活化与CD14的表达有关，CD14是LPS和其他微生物产物的高亲和力受体，Toll样受体2是Toll家族受体的一员，最近与革兰氏阳性菌的宿主反应有关。与亲本菌株相反，合成的LPS拮抗剂E5564不抑制LPS缺陷型突变体。我们的结论是，即使在LPS的情况下，革兰氏阴性细胞壁仍然是一个有效的炎症刺激剂，利用信号通路摇摆独立于那些参与LPS信号。
The recent isolation of a lipopolysaccharide (LPS)-deficient mutant of Neisseria meningitidis has allowed us to explore the roles of other gram-negative cell wall components in the host response to infection. The experiments in this study were designed to examine the ability of this mutant strain to activate cells. Although it was clearly less potent than the parental strain, we found the LPS-deficient mutant to be a capable inducer of the inflammatory response in monocytic cells, inducing a response similar to that seen with Staphylococcus aureus. Cellular activation by the LPS mutant was related to expression of CD14, a high-affinity receptor for LPS and other microbial products, as well as Toll-like receptor 2, a member of the Toll family of receptors recently implicated in host responses to gram positive bacteria. In contrast to the parental strain, the synthetic LPS antagonist E5564 did not inhibit the LPS-deficient mutant. We conclude that even in the absence of LPS, the gram-negative cell wall remains a potent inflammatory stimulant, utilizing signaling path wags independent of those involved in LPS signaling.