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

LS Miller, RM O'Connell, MA Gutierrez, EM Pietras… - Immunity, 2006 - cell.com
LS Miller, RM O'Connell, MA Gutierrez, EM Pietras, A Shahangian, CE Gross, A Thirumala…
Immunity, 2006cell.com
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-1R-deficient mice were
substantially larger with higher bacterial counts compared with wild-type mice. In contrast,
TLR2-deficient mice had lesions that were only moderately larger with minimally higher …
Summary
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-1R-deficient mice were substantially larger with higher bacterial counts compared with wild-type 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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