Toll-like receptor 4 dependence of innate and adaptive immunity to Salmonella:: Importance of the Kupffer cell network

被引:128
作者
Vazquez-Torres, A
Vallance, BA
Bergman, MA
Finlay, BB
Cookson, BT
Jones-Carson, J
Fang, FC
机构
[1] Univ Washington, Sch Med, Dept Microbiol, Seattle, WA 98195 USA
[2] Univ Washington, Sch Med, Dept Lab Med, Seattle, WA 98195 USA
[3] Univ Colorado, Hlth Sci Ctr, Dept Microbiol, Denver, CO 80262 USA
[4] Univ British Columbia, Biotechnol Lab, Vancouver, BC V5Z 1M9, Canada
关键词
D O I
10.4049/jimmunol.172.10.6202
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Mammalian cells recognize LPS from Gram-negative bacteria via the Toll-like receptor 4 (TLR4) complex. During experimental Salmonella infection, C3H/HeJ mice carrying a dominant-negative mutation in TLR4 exhibited delayed chemokine production, impaired NO generation, and attenuated cellular immune responses. However, dramatically enhanced bacterial growth within the Kupffer cell network before the recruitment of inflammatory cells appeared to be primarily responsible for the early demise of Salmonella-infected TLR4-deficient mice. LPS-TLR4 signaling plays an essential role in the generation of both innate and adaptive immune responses throughout the course of infection with Gram-negative bacteria. Alternative pattern-recognition receptors cannot completely compensate for the loss of TLR4, and compensation occurs at the expense of an increased microbial burden.
引用
收藏
页码:6202 / 6208
页数:7
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