Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 136, Issue 3, Pages 621-630Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2015.12.024
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Funding
- National Natural Science Foundation of China [31222021, 31470878, 31100109, 31170867]
- Science and Technology Commission of Shanghai Municipality [13JC1402301, 11DZ2260300]
- Shanghai Education Commission [13SG25]
- New Century Excellent Talents in University [NCET-11-0141]
- Henry Fok Educational Foundation [141017]
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4 Staphylococcus epidermidis (S. epidermidis) plays a critical role in modulating cutaneous inflammatory responses in skin. Although S. epidermidis has been shown to co-colonize with Propionibacterium acnes (P. acnes) in acne lesions, it is unclear whether S. epidermidis is involved in the regulation of P. acnes-induced inflammatory responses. In this study, we demonstrated that S. epidermidis inhibited P. acnes-induced inflammation in skin. P. acnes induced the expression of interleukin-6 and tumor necrosis factor-a via the activation of toll-like receptor (TLR) 2 in both keratinocytes and mouse ears. Staphylococcal lipoteichoic acid activated TLR2 to induce miR-143 in keratinocytes, and miR-143, in turn, directly targeted 30 UTR of TLR2 to decrease the stability of TLR2 mRNA and then decreased TLR2 protein, thus inhibiting P. acnes-induced proinflammatory cytokines. The inhibitory effect of miR-143 was further confirmed in vivo as the administration of miR-143 antagomir into mouse ears abrogated the inhibitory effect of lipoteichoic acid on P. acnes-induced inflammation in skin. Taken together, these observations demonstrate that staphylococcal lipoteichoic acid inhibits P. acnes-induced inflammation via the induction of miR-143, and suggest that local modulation of inflammatory responses by S. epidermidis at the site of acne vulgaris might be a beneficial therapeutic strategy for management of P. acnes-induced inflammation.
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