한빛사논문
- 조회265
Hyo Jeong Kim 1,3, Yun Sang Lee 1,3, Bok-Soon Lee 1, Chang-Hak Han 1,2, Sang Gyu Kim 1,2 and Chul-Ho Kim 1,2,*
1Department of Otolaryngology, School of Medicine, Ajou University, Suwon, Republic of Korea.
2Department of Molecular Science and Technology, Ajou University, Suwon, Republic of Korea.
3These authors contributed equally: Hyo Jeong Kim, Yun Sang Lee
*Corresponding author: correspondence to Chul-Ho Kim
Abstract
Inflammasomes are multiprotein complexes involved in the host immune response to pathogen infections. Thus, inflammasomes participate in many conditions, such as acne. Recently, it was shown that NETosis, a type of neutrophil cell death, is induced by bacterial infection and is involved in inflammatory diseases such as delayed wound healing in patients with diabetes. However, the relationship between inflammasomes and NETosis in the pathogenesis of inflammatory diseases has not been well studied. In this study, we determined whether NETosis is induced in P. acnes-induced skin inflammation and whether activation of the nucleotide-binding domain, leucine-rich family, and pyrin domain-containing-3 (NLRP3) inflammasome is one of the key factors involved in NETosis induction in a mouse model of acne skin inflammation. We found that NETosis was induced in P. acnes-induced skin inflammation in mice and that inhibition of NETosis ameliorated P. acnes-induced skin inflammation. In addition, our results demonstrated that inhibiting inflammasome activation could suppress NETosis induction in mouse skin. These results indicate that inflammasomes and NETosis can interact with each other to induce P. acnes-induced skin inflammation and suggest that targeting NETosis could be a potential treatment for inflammasome-mediated diseases as well as NETosis-related diseases.
논문정보
- Research article
- 2024년 02월 (BRIC 등록일 2024-03-13)
- 국내 연구진
- 의약학 > 종양의학
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