Mucosal immunity and microbiota change in the rainbow trout (Oncorhynchus mykiss) gills after being challenged with infectious hematopoietic necrosis virus

传染性造血坏死病毒 生物 虹鳟 微生物学 先天免疫系统 免疫 鳟鱼 免疫系统 粘液 失调 病毒 病毒学 免疫学 肠道菌群 生态学 渔业
作者
Pajongjit Tongsri,Gaofeng Cheng,Zhenyu Huang,Zixuan Wang,Fen Dong,Zhengben Wu,Weiguang Kong,Yongyao Yu,Zhen Xu
出处
期刊:Fish & Shellfish Immunology [Elsevier BV]
卷期号:142: 109166-109166 被引量:4
标识
DOI:10.1016/j.fsi.2023.109166
摘要

Respiratory structures are crucial for vertebrate survival, as they serve not only to perform gas-exchange processes but also as entry points for opportunistic pathogens. Previous studies have demonstrated that fish contain gill mucosal-associated lymphoid tissue, and harbor a large number of commensal bacteria on their surface and contribute to maintaining fish health. However, by far, very limited information is known regarding the effects of viral infection on gill mucosal immunity and microbiota homeostasis. In this study, we conducted an infection model by bath with infectious hematopoietic necrosis virus (IHNV) and revealed a 27 % mortality rate among rainbow trout in the first two weeks after infection. Moreover, we found that diseased fish with the highest IHNV loads in gills exhibiting severe damage, as well as increased goblet cell counts in both primary lamellae (PL) and secondary lamellae (SL). Additionally, RT-qPCR and RNA-seq analyses revealed that IHNV infection induced a strong innate and adaptive antiviral immune responses. Interestingly, an antibacterial immune response was also observed, suggesting that a secondary bacterial infection occurred in trout gills after viral infection. Furthermore, 16S rRNA analysis of trout gills revealed a profound dysbiosis marked by a loss of beneficial taxa and expansion of pathobionts following IHNV infection. Overall, our finding demonstrates that IHNV infection induces significant changes of the microbial community in the fish respiratory surface, thus triggering local antiviral and bacterial mucosal immunity.
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