TLR2-Dependent Inflammatory Response to Porphyromonas gingivalis Is MyD88 Independent, whereas MyD88 Is Required To Clear Infection

被引:63
作者
Burns, Elia [1 ]
Eliyahu, Tal [1 ]
Uematsu, Satoshi [2 ]
Akira, Shizuo [2 ]
Nussbaum, Gabriel [1 ]
机构
[1] Hadassah & Hebrew Univ, Med Ctr, Fac Med Dent, Inst Dent Sci, Jerusalem, Israel
[2] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Osaka, Japan
基金
以色列科学基金会;
关键词
TOLL-LIKE RECEPTOR-2; NF-KAPPA-B; DOMAIN-CONTAINING ADAPTERS; INNATE IMMUNE-RESPONSE; CELL-WALL COMPONENTS; SIGNALING PATHWAYS; CUTTING EDGE; PHAGOSOME MATURATION; CHLAMYDIA-PNEUMONIAE; PULMONARY INFECTION;
D O I
10.4049/jimmunol.0900378
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Porphyromonas gingivalis is a Gram-negative anaerobe considered to be a major periodontal pathogen. TLR2 plays a central role in the response to P gingivalis infection in vivo. In its absence there is a weak inflammatory response; however, bacteria are cleared rapidly compared with wild-type mice. We examined the role of the TLR adaptor proteins MyD88 and TLR/IL-1R-domain-containing adaptor-inducing IFN-beta in the inflammatory response to P gingivalis in vivo and in the ability to clear the bacterial infection. Proinflammatory cytokine production in response to P gingivalis infection depends on TLR2, but it does not require MyD88 or TLR/IL-1R-domain-containing adaptor-inducing IFN-beta. In contrast, the generation of intracellular toxic oxygen species and the ultimate clearance of P gingivalis infection depend critically on MyD88, independent of TLR2. Thus, robust cytokine production and bacterial clearance are independent events mediated by distinct signaling pathways following infection with P. gingivalis. The Journal of Immunology, 2010, 184: 1455-1462.
引用
收藏
页码:1455 / 1462
页数:8
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