4.7 Article

Epinephelus coioides Hsp27 negatively regulates innate immune response and apoptosis induced by Singapore grouper iridovirus (SGIV) infection

期刊

FISH & SHELLFISH IMMUNOLOGY
卷 120, 期 -, 页码 470-480

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fsi.2021.12.016

关键词

Epinephelus coioides; Hsp27; SGIV; Virus replication; Immune response

资金

  1. National Natural Science Foundation of China [U20A20102, 31930115]
  2. Innovation Group Project of Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai) [311021006]
  3. China Agriculture Research System of MOF and MARA [CARS-47-G16]
  4. Marine Fisheries Bureau Key funds and marine projects [GDME-2018C002]
  5. National Key R&D Program of China [2018YFD0900501, 2018YFC0311302]
  6. National key research and development plan subject [2019YFD0900801]
  7. foundation of key Lab-oratory of Tropical Marine Bio-resources and Ecology, Chinese Academy of Sciences [2019011008]
  8. Hainan Key Laboratory of Tropical Marine Biotechnology [LTMB201902]
  9. Natural Foundation of Guang-dong Province to Hong-Yan Sun

向作者/读者索取更多资源

The study characterized Hsp27 of Epinephelus coioides and found that it may play a role in SGIV infection by negatively regulating the innate immune response.
Heat shock proteins (Hsps) are important for maintaining protein homeostasis and cell survival. In this study, Hsp27 of Epinephelus coioides, an economically important marine fish in China and Southeast Asian countries, was characterized. E. coioides Hsp27 contains the consered ACD_HspB1_like domain and three p38 MAPK phosphorylation sites, located at Thr-13, Thr-60 and Ser-167. E. coioides Hsp27 was distributed in both the cytoplasm and nucleus, its mRNA was detected in all 14 tissues examined, and its expression was up-regulated after challenge with Singapore grouper iridovirus (SGIV), an important E. coioides pathogen. Over-expression of E. coioides Hsp27 significantly upregulated the expressions of the key SGIV genes (VP19, LITAF, MCP, and ICP18), downgraded the expressions of the E. coioides immune factors (IRF3, IRF7, ISG15, and TRAF6) and proinflammatory factors (TNF-alpha, IL-8), downgraded the activation of nuclear factor kappa-B (NF-kappa B) and activator protein-1 (AP-1), and substantially inhibited the cell apoptosis induced by SGIV infection. These data illustrated that E. coioides Hsp27 might be involved in SGIV infection by negatively regulating the innate immune response.

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