Journal
IMMUNITY
Volume 24, Issue 1, Pages 79-91Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2005.11.011
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Funding
- NCI NIH HHS [R01 CA87924] Funding Source: Medline
- NIAID NIH HHS [R01 AI22553, R01 AI056154, R01 AI47868, K08 AI62985, R01 AI052359] Funding Source: Medline
- NIAMS NIH HHS [R01 AR40312] Funding Source: Medline
- NIGMS NIH HHS [GM 07185] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA087924] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI022553, K08AI062985, R37AI047868, R01AI052359, R01AI056154, R01AI047868, R22AI022553] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR040312] Funding Source: NIH RePORTER
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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.
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