MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus
MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus
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DOI：
10.1016/j.immuni.2005.11.011
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发表时间：
2006-01-01
期刊：
影响因子：
32.4
通讯作者：
Modlin, RL
中科院分区：
文献类型：
--
作者：
Miller, LS;O'Connell, RM;Modlin, RL
MyD88 是 TLR 和 IL-1R 家族成员的重要信号转导接头。在这里，我们通过使用皮肤感染模型与生物发光细菌结合评估了 TLR2/MyD88 和 IL-1R/MyD88 信号在宿主防御金黄色葡萄球菌中的作用。我们发现，与野生型小鼠相比，金黄色葡萄球菌感染的MyD88和IL-1R缺陷型小鼠的病变明显更大，并且细菌计数更高。相比之下，TLR2缺陷小鼠的病变仅稍大一些，细菌计数也稍高一些。此外，MyD88-和IL-1R-而非TLR2缺陷小鼠的中性粒细胞向感染部位的募集严重减少。这种中性粒细胞的募集并不依赖于募集的骨髓来源细胞的 IL-1R/MyD88 信号传导，表明常驻皮肤细胞利用 IL-1R/MyD88 信号传导来促进中性粒细胞募集。
MyD88 is an important signaling adaptor for both TLR and IL-1R family members. Here, we evaluated the role of TLR2/MyD88 and IL-1R/MyD88 signaling in host defense against S. aureus by using a cutaneous infection model in conjunction with bioluminescent bacteria. We found that lesions of S. aureus-infected MyD88- and IL-lR-deficient mice were substantially larger with higher bacterial counts compared with wildtype mice. In contrast, TLR2-deficient mice had lesions that were only moderately larger with minimally higher bacterial counts. In addition, MyD88- and IL-1R- but not TLR2-deficient mice had severely decreased recruitment of neutrophils to the site of infection. This neutrophil recruitment was not dependent upon IL-1R/MyD88 signaling by recruited bone marrow-derived cells, suggesting that resident skin cells utilize IL-1R/MyD88 signaling to promote neutrophil recruitment.