2. Academic Validation
  3. Triclocarban evoked neutrophil extracellular trap formation in common carp (Cyprinus carpio L.) by modulating SIRT3-mediated ROS crosstalk with ERK1/2/p38 signaling

Triclocarban evoked neutrophil extracellular trap formation in common carp (Cyprinus carpio L.) by modulating SIRT3-mediated ROS crosstalk with ERK1/2/p38 signaling

  • Fish Shellfish Immunol. 2022 Oct;129:85-95. doi: 10.1016/j.fsi.2022.08.060.
Siwen Li 1,  Yanling Wang 2,  Dongke Yu 3,  Yuan Zhang 3,  Xiali Wang 4,  Mei Shi 2,  Yanxin Xiao 2,  Xinlian Li 2,  Hongtao Xiao 5,  Lu Chen 6,  Xuan Xiong 7
Affiliations

Affiliations

  • 1 Xiangya School of Public Health, Central South University, Changsha, 410078, Hunan Province, PR China.
  • 2 College of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuan Province, PR China.
  • 3 Department of Pharmacy, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan Province, PR China; Personalized Drug Therapy Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan Province, PR China.
  • 4 College of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuan Province, PR China; Department of Child Healthcare, Luzhou Longmatan District Maternal and Child Health Care Hospital, Luzhou, 646000, Sichuan Province, PR China.
  • 5 Department of Pharmacy, Sichuan Cancer Hospital & Institute, The Affiliated Cancer Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610089, Sichuan Province, PR China. Electronic address: xiongxuan@med.uestc.edu.cn.
  • 6 Department of Pharmacy, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan Province, PR China; Personalized Drug Therapy Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan Province, PR China. Electronic address: llilychen2006@163.com.
  • 7 Department of Pharmacy, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan Province, PR China; Personalized Drug Therapy Key Laboratory of Sichuan Province, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610072, Sichuan Province, PR China. Electronic address: xht927@163.com.
PMID: 36057428 DOI: 10.1016/j.fsi.2022.08.060
Abstract

Triclocarban (TCC), an antimicrobial ingredient in personal care products, is associated with immunosuppression and physiological dysfunctions of aquatic organisms. The aim of this study was to investigate whether TCC can induce common carp NETosis (neutrophil death by neutrophil extracellular trap (NET) release) and then to attempt to identify the potential molecular mechanisms. Herein, scanning electron microscopy and flow cytometric assays showed that revealed that TCC triggers DNA-containing web-like structures and increases extracellular DNA content. In the proteomic analysis, we observed that NET-related proteins, extracellular regulated protein kinase (Mapk1, Mapk14, JAK2) and apoptotic protein (caspase3) were significantly increased, and defender against cell death 1 (Dad1) was significantly decreased after TCC treatments. Meanwhile, we confirmed that TCC stress can trigger NETosis in common carp by activating the Reactive Oxygen Species (ROS)/ERK1/2/p38 signaling. We think that the upregulated NDUFS1 expression is closely related to oxidative stress induced by TCC. Importantly, we discovered that SIRT3 expression was significantly decreased in the process of TCC-induced NETs. Importantly, pretreatment with the SIRT3 agonist honokiol (HKL) effectively suppressed TCC-induced NET release. In contrast, the SIRT3 antagonist 3-TYP escalated TCC-induced NET formation. Mechanistically, SIRT3 degradation serves as a potential mediator for regulating oxidative stress crosstalk between ERK1/2/p38 signals in the process of TCC-induced NET formation. These findings unveil new insights into the TCC-evoked health risk of fish and other aquatic organisms and suggest that SIRT3 is a potential pharmacological intervention target to alleviate TCC-induced common carp NETosis.

Keywords

Common carp; Neutrophil extracellular traps (NETs); Reactive oxygen species (ROS); SIRT3; Triclocarban (TCC).

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