Fish decay-accelerating factor (DAF) regulates intestinal complement pathway and immune response to bacterial challenge
文献类型: 外文期刊
作者: Xia Zhang;Yuhan Zhang;Ting Wu;Hao He;Ran Peng;Kelan Jin;Huilan Mo;Fufa Qu;Jianzhou Tang;Yonghua Zhou;Yalin Yang;Zhigang Zhou;Junde Fan;Jianzhong Li;Zhen Liu
作者机构:
关键词: Ctenopharyngodon idella;Decay-accelerating factor;Intestinal immunity;Lipopolysaccharide;Muramyl dipeptide
期刊名称: Fish and Shellfish Immunology
ISSN: 1050-4648
年卷期: 2024 年 151 卷
页码:
收录情况: SCIE(2024版)
摘要: Decay-accelerating factor (DAF) is an essential member of the complement regulatory protein family that plays an important role in immune response and host homeostasis in mammals. However, the immune function of DAF has not been well characterized in bony fish. In this study, a complement regulatory protein named CiDAF was firstly characterized from Ctenopharyngodon idella and its potential roles were investigated in intestine following bacterial infection. Similar to mammalian DAFs, CiDAF has multiple complement control protein (CCP) functional domains, suggesting the evolutionary conservation of DAFs. CiDAF was broadly expressed in all tested tissues, with a relatively high expression level detected in the spleen and kidney. In vivo immune challenge experiments revealed that CiDAF strongly responded to bacterial pathogens (Aeromonas hydrophila and Aeromonas veronii) and PAMPs (lipopolysaccharide (LPS) or muramyl dipeptide (MDP)) challenges. In vitro RNAi experiments indicated that knockdown of CiDAF could upregulate the expression of complement genes (C4b, C5 and C7) and inflammatory cytokines (TNF-α, IL-1β and IL-8). Moreover, 2000 ng/mL of CiDAF agonist progesterone effectively alleviated LPS- or MDP-induced intestinal inflammation by regulating expression of complement factors, TLR/PepT1 pathway genes and inflammatory cytokines. Overall, these findings revealed that CiDAF may act as a negative regulator of intestinal complement pathway and immune response to bacterial challenge in grass carp.
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