MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus

被引:273
作者
Miller, LS
O'Connell, RM
Gutierrez, MA
Pietras, EM
Shahangian, A
Gross, CE
Thirumala, A
Cheung, AL
Cheng, GH
Modlin, RL
机构
[1] Univ Calif Los Angeles, Div Dermatol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Dept Microbiol Immunol & Mol Genet, David Geffen Sch Med, Los Angeles, CA 90095 USA
[3] Dartmouth Coll Sch Med, Dept Microbiol & Immunol, Hanover, NH 03755 USA
关键词
D O I
10.1016/j.immuni.2005.11.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:79 / 91
页数:13
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