期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 140, 期 5, 页码 1066-+出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2019.11.016
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资金
- Doris Duke Foundation
- National Institutes of Health National Institute of Arthritis and Musculoskeletal and Skin disease [R01 AR071384, R03 AR-066337-01-A1]
- University of Michigan Skin Biology and Diseases Resources-based Center [1P30AR075043]
- Applied Systems Biology Core in the O'Brien Renal Center [P30 DK081943]
- NIH [AI133089]
- Department of Veteran Affairs [BX002711]
- U.S. Department of Veterans Affairs
- University of Michigan Sequencing Core facility
- University of Michigan Microscopy Core facility
Cutaneous inflammation is recurrent in systemic lupus erythematosus (SLE), yet mechanisms that drive cutaneous inflammation in SLE are not well defined. Type I IFNs are elevated in nonlesional SLE skin and promote inflammatory responses. Staphylococcus aureus, known to induce IFN production, could play a role in cutaneous inflammation in SLE. We show here that active cutaneous lupus erythematosus lesions are highly colonized (w50%) by S. aureus. To define the impact of IFNs on S. aureus colonization, we examined the effects of type I and type II IFNs on S. aureus adherence and invasion. An increase in adherent S. aureus was observed after exposure to both IFN-a and-g, whereas IFN-g appeared to inhibit invasion of S. aureus. Cutaneous lupus erythematosus lesional skin microarray data and RNA sequencing data from SLE keratinocytes identified repression of barrier gene expression, such as filaggrin and loricrin, and SLE keratinocytes exhibited increased S. aureusebinding integrins. These SLE-associated changes could be replicated by IFN treatment of keratinocytes. Further, SLE keratinocytes exhibited increased binding to S. aureus. Together, these data suggest that chronic exposure to IFNs induces barrier disruption that allows for higher S. aureus colonization in SLE skin.
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