Induction of a novel mechanism of accelerated bacterial clearance by lipopolysaccharide in CD14-deficient and toll-like receptor 4-deficient mice
Induction of a novel mechanism of accelerated bacterial clearance by lipopolysaccharide in CD14-deficient and toll-like receptor 4-deficient mice
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DOI：
10.4049/jimmunol.166.2.1075
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发表时间：
2001-01-15
影响因子：
4.4
通讯作者：
Goyert, SM
中科院分区：
文献类型：
--
作者：
Haziot, A;Hijiya, N;Goyert, SM
尽管缺乏对LPS的促炎反应，但CD 14缺陷小鼠清除革兰氏阴性细菌（大肠杆菌0111）的效率比正常小鼠高至少10倍。在这项研究中，我们表明，这是由于早期和激烈的招聘中性粒细胞后，注射革兰氏阴性菌或LPS的CD 14缺陷小鼠;相比之下，中性粒细胞浸润延迟24小时，在正常小鼠。早期LPS诱导的PMN浸润和E.在Toll样受体（TLR）4缺陷型小鼠中观察到了大肠杆菌。此外，LPS的脂质A部分不仅在CD 14缺陷和TLR-4缺陷小鼠中诱导早期中性粒细胞浸润，而且在正常小鼠中也诱导早期中性粒细胞浸润。总之，LPS的脂质A组分刺激先天免疫应答的独特和关键途径，其独立于CD 14和TLR 4，并导致早期中性粒细胞浸润和增强的细菌清除。
Despite the lack of a proinflammatory response to LPS, CD14-deficient mice clear Gram-negative bacteria (Escherichia coli 0111) at least 10 times more efficiently than normal mice. In this study, we show that this is due to an early and intense recruitment of neutrophils following the injection of Gram-negative bacteria or LPS in CD14-deficient mice; in contrast, neutrophil infiltration is delayed by 24 h in normal mice. Similar results of early LPS-induced PMN infiltration and enhanced clearance of E. coli were seen in Toll-like receptor (TLR) 4-deficient mice. Furthermore, the lipid A moiety of LPS inducted early neutrophil infiltration not only in CD14-deficient and TLR-4-deficient mice, but also in normal mice. In conclusion, the lipid A component of LPS stimulates a unique and critical pathway of innate immune responses that is independent of CD14 and TLR4 and results in early neutrophil infiltration and enhanced bacterial clearance.