1. Academic Validation
  2. Antimicrobial peptide-producing dermal preadipocytes defend against Candida albicans skin infection via the FGFR-MEK-ERK pathway

Antimicrobial peptide-producing dermal preadipocytes defend against Candida albicans skin infection via the FGFR-MEK-ERK pathway

  • PLoS Pathog. 2023 Nov 30;19(11):e1011754. doi: 10.1371/journal.ppat.1011754.
Jianing Wang 1 Zhimin Duan 1 Rong Zeng 1 Lu Yang 1 Weizhao Liu 2 Yiman Liu 3 Qian Yao 3 Xu Chen 1 2 Ling-Juan Zhang 3 Min Li 1 2
Affiliations

Affiliations

  • 1 Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and Sexually Transmitted Infections, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China.
  • 2 School of Public Health, Nanjing Medical University, Nanjing, China.
  • 3 State Key Laboratory of Cellular Stress Biology, School of Pharmaceutical Sciences, Xiamen University, Xiamen, China.
Abstract

Dermal fibroblasts (dFBs) defend against deep Bacterial skin infections by differentiating into preadipocytes (pAds) that produce the antimicrobial peptide cathelicidin; this differentiation is known as the dermal reactive adipogenesis response. However, the role of dFBs in fungal Infection remains unknown. Here, we found that cathelicidin-producing pAds were present in high numbers in skin lesions from patients with cutaneous Candida granulomas. Second, we showed that dermal Candida albicans (C. albicans) Infection in mice robustly triggered the dermal reactive adipogenesis response and induced cathelicidin expression, and inhibition of adipogenesis with pharmacological inhibitors of Peroxisome Proliferator-activated Receptor γ (PPARγ) impaired skin resistance to C. albicans. In vitro, C. albicans products induced cathelicidin expression in pAds, and differentiating pAds markedly suppressed the growth of C. albicans by producing cathelicidin. Finally, we showed that C. albicans induced an antimicrobial response in pAds through the FGFR-MEK-ERK pathway. Together, our data reveal a previously unknown role of dFBs in the defense against skin Infection caused by C. albicans.

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    99.85%, FGFR抑制剂