| Literature DB >> 30594464 |
Ling-Juan Zhang1, Stella Xiang Chen2, Christian F Guerrero-Juarez3, Fengwu Li2, Yun Tong2, Yuqiong Liang4, Marc Liggins2, Xu Chen5, Hao Chen5, Min Li5, Tissa Hata2, Ye Zheng4, Maksim V Plikus3, Richard L Gallo6.
Abstract
Dermal fibroblasts (dFBs) resist infection by locally differentiating into adipocytes and producing cathelicidin antimicrobial peptide in response to Staphylococcus aureus (S. aureus). Here, we show that neonatal skin was enriched with adipogenic dFBs and immature dermal fat that highly expressed cathelicidin. The pool of adipogenic and antimicrobial dFBs declined after birth, leading to an age-dependent loss of dermal fat and a decrease in adipogenesis and cathelidicin production in response to infection. Transforming growth factor beta (TGF-β), which acted on uncommitted embryonic and adult dFBs and inhibited their adipogenic and antimicrobial function, was identified as a key upstream regulator of this process. Furthermore, inhibition of the TGF-β receptor restored the adipogenic and antimicrobial function of dFBs in culture and increased resistance of adult mice to S. aureus infection. These results provide insight into changes that occur in the skin innate immune system between the perinatal and adult periods of life.Entities:
Keywords: Staphylococcus aureus; adipocyte progenitors; adipocytes; antimicrobial peptides; cathelicidin; dermal fibroblasts; dermal white adipose tissue; infection; innate immunity; transforming growth factor beta
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Year: 2018 PMID： 30594464 PMCID： PMC7191997 DOI： 10.1016/j.immuni.2018.11.003
Source DB: PubMed Journal: Immunity ISSN： 1074-7613 Impact factor: 31.745