2. Academic Validation
  3. TRPV3 promotes sebocyte inflammation via transcriptional modulating TLR2 in acne

TRPV3 promotes sebocyte inflammation via transcriptional modulating TLR2 in acne

  • Biochim Biophys Acta Mol Basis Dis. 2024 Apr 20;1870(5):167195. doi: 10.1016/j.bbadis.2024.167195.
Ziyu Wei 1,  Meng Gao 1,  Yihe Liu 1,  Rong Zeng 2,  Juan Liu 3,  Shuya Sun 1,  Siyuan Li 1,  Linghan Hu 1,  Ruiyu Xiang 1,  Ran Mo 1,  Zhongya Song 1,  Zhiming Chen 1,  Dan Bao 2,  Di Hua 1,  Christos C Zouboulis 4,  Yanyan Feng 5,  Ji Li 6,  Yong Yang 7
Affiliations

Affiliations

  • 1 Genetic Skin Disease Center, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China.
  • 2 Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, Jiangsu, China.
  • 3 Department of Dermatology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • 4 Departments of Dermatology, Venereology, Allergology and Immunology, Staedtisches Klinikum Dessau, Brandenburg Medical School Theodor Fontane, Faculty of Health Sciences Brandenburg, Dessau, Germany.
  • 5 Department of Dermatology, Chengdu Second People's Hospital, Chengdu, Sichuan, China.
  • 6 Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
  • 7 Genetic Skin Disease Center, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China. Electronic address: yyang@pumcderm.cams.cn.
PMID: 38648901 DOI: 10.1016/j.bbadis.2024.167195
Abstract

Acne is a common chronic inflammatory disease of the pilosebaceous unit. Transient receptor potential vanilloid 3 (TRPV3) is an ion channel that is involved in inflammatory dermatosis development. However, the involvement of TRPV3 in acne-related inflammation remains unclear. Here, we used acne-like mice and human sebocytes to examine the role of TRPV3 in the development of acne. We found that TRPV3 expression increased in the skin lesions of Propionibacterium acnes (P. acnes)-injected acne-like mice and the facial sebaceous glands (SGs) of acne patients. TRPV3 promoted inflammatory cytokines and chemokines secretion in human sebocytes and led to neutrophil infiltration surrounding the SGs in acne lesions, further exacerbating sebaceous inflammation and participating in acne development. Mechanistically, TRPV3 enhanced TLR2 level by promoting transcriptional factor phosphorylated-FOS-like antigen-1 (p-FOSL1) expression and its binding to the TLR2 promoter, leading to TLR2 upregulation and downstream NF-κB signaling activation. Genetic or pharmacological inhibition of TRPV3 both alleviated acne-like skin inflammation in mice via the TLR2-NF-κB axis. Thus, our study revealed the critical role of TRPV3 in sebaceous inflammation and indicated its potential as an acne therapeutic target.

Keywords

Acne vulgaris; Chemotaxis; Inflammation; P. acnes; Sebocytes; TRPV3.

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