2. Academic Validation
  3. Immunosuppression participated in complement activation-mediated inflammatory injury caused by 4-octylphenol via TLR7/IκBα/NF-κB pathway in common carp (Cyprinus carpio) gills

Immunosuppression participated in complement activation-mediated inflammatory injury caused by 4-octylphenol via TLR7/IκBα/NF-κB pathway in common carp (Cyprinus carpio) gills

  • Aquat Toxicol. 2022 Aug:249:106211. doi: 10.1016/j.aquatox.2022.106211.
Qi Sun 1,  Yuhao Liu 1,  Xiaojie Teng 2,  Peng Luan 1,  Xiaohua Teng 3,  Xiujie Yin 4
Affiliations

Affiliations

  • 1 College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China.
  • 2 Grassland Station in Heilongjiang Province, Harbin 150067, China.
  • 3 College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China. Electronic address: tengxiaohua@neau.edu.cn.
  • 4 College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, China. Electronic address: yinxiujie@neau.edu.cn.
PMID: 35667248 DOI: 10.1016/j.aquatox.2022.106211
Abstract

4-octylphenol (4-OP), a toxic estrogenic environmental pollutant, can threaten aquatic animal and human health. However, toxic effect of 4-OP on fish has not been reported. To investigate molecular mechanism of gill poisoning caused by 4-OP exposure, a carp 4-OP poisoning model was established, and then blood and gills were collected on day 60. The results demonstrated that gill was a target organ attacked by 4-OP, and exposure to 4-OP caused carp gill inflammatory injury. There were 1605 differentially expressed genes (DEGs, including 898 up-regulated DEGs and 707 down-regulated DEGs). KEGG and GO were used to further analyze obtained 1605 DEGs, indicating that complement activation, immune response, and inflammatory response participated in the mechanism of 4-OP-caused carp gill inflammatory injury. Our data at transcription level further revealed that 4-OP caused complement activation through triggering Complement Component 3a/Complement Component 3a receptor (C3a/C3aR) axis and Complement Component 5a/Complement Component 5a receptor 1 (C5a/C5aR1) axis, induced immunosuppression through the imbalances of T helper (Th) 1/Th2 cells and regulatory T (Treg)/Th17 cells, as well as caused inflammatory injury via toll like receptor 7/inhibitor kappa B alpha/nuclear factor-kappa B (TLR7/IκBα/NF-κB) pathway. Taken together, immunosuppression participated in complement activation-mediated inflammatory damage in carp gills after 4-OP treatment. The findings of this study will provide pioneering information and theoretical support for the mechanism of 4-OP poisoning, and will provide reference for the assessment of estrogenic environmental pollution risk.

Keywords

4-OP; Complement activation; Immunosuppression; Inflammatory injury; Transcriptome analysis.

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