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

Lloyd S. Miller, Ryan M. O'Connell, Miguel A. Gutierrez, Eric M. Pietras, Arash Shahangian, Catherine E. Gross, Ajaykumar Thirumala, Ambrose L. Cheung, Genhong Cheng, Robert L. Modlin

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)79-91
Number of pages13
JournalImmunity
Volume24
Issue number1
DOIs
StatePublished - Jan 1 2006
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Fingerprint Dive into the research topics of 'MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus'. Together they form a unique fingerprint.

  • Cite this

    Miller, L. S., O'Connell, R. M., Gutierrez, M. A., Pietras, E. M., Shahangian, A., Gross, C. E., Thirumala, A., Cheung, A. L., Cheng, G., & Modlin, R. L. (2006). MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus. Immunity, 24(1), 79-91. https://doi.org/10.1016/j.immuni.2005.11.011