期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 130, 期 7, 页码 1866-1876出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2010.37
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资金
- National Institutes of Health [AR053672]
- American Heart Association [0535212N]
- Transdisciplinary Program in Translational Medicine and Therapeutics at the University of Pennsylvania
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [0918934] Funding Source: National Science Foundation
Staphylococcus aureus is a significant human pathogen that can colonize the skin. Neutrophils are well known to be involved in clearance of the bacterium. This study focused on exploring the role that human keratinocytes have as first responders to bacterial challenges. IL-1 alpha and IL-1 beta increased mRNA production and protein secretion of the neutrophil chemotactic CXCL1, CXCL2, and IL-8 in keratinocytes. S. aureus and the bacterial cell wall components lipoteichoic acid (LTA) and peptidoglycan (PGN) induced similar expression profiles in a Toll-like receptor (TLR)-2-dependent manner. Interestingly, the S. aureus-induced mRNA levels peaked at later time points than those induced by IL-1. The S. aureus-activated chemokine production was preceded by significant IL-1 alpha and IL-1 beta secretion. Expression of IL-1 alpha was significantly higher than that of IL-1 beta. Inhibition of IL-1RI using neutralizing antibodies revealed that S. aureus-derived LTA and PGN-induced chemokine expression requires IL-1RI engagement. Surprisingly, we further found that chemokine secretion is dependent upon endocrine IL-1 alpha, but not IL-1 beta, signaling. Our data show that the innate immune response of keratinocytes is regulated differently than those of other cell types. This may represent a fail-safe system that protects the host against genetic variation and immune evasion mechanisms developed by pathogens.
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