Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 128, Issue 8, Pages 1964-1968Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2008.27
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Funding
- NIAID NIH HHS [R56 AI090863, AI 060840] Funding Source: Medline
- NIAMS NIH HHS [R01 AR052728] Funding Source: Medline
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Skin, the first barrier against invading microorganisms, is hypoxic, even under baseline conditions. The transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha, the principal regulator of cellular adaptation to low oxygen, is strongly expressed in skin epithelium. HIF-1 alpha is now understood to play a key role in the bactericidal capacity of phagocytic cells such as macrophages and neutrophils. In the skin, keratinocytes provide a direct antibacterial activity through production of antimicrobial peptides, including cathelicidin. Here, we generate mice with a keratinocyte-specific deletion of HIF-1 alpha and examine effects on intrinsic skin immunity. Keratinocyte HIF-1 alpha is seen to provide protection against necrotic skin lesions produced by the pathogen group A Streptococcus. RNA interference studies reveal that HIF-1 alpha regulation of keratinocyte cathelicidin production is critical to their antibacterial function.
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