Immune Suppression and Rapid Invasion of Nile Tilapia Gills Following an Acute Challenge by <i>Flavobacterium davisii</i>
Yingxuan Xu,
Shifeng Wang,
Yongcan Zhou,
Zhenyu Xie,
Bei Wang,
Zhangding Zhao,
Wenlong Cai,
Peibo Wang,
Weiliang Guo,
Dongdong Zhang,
Zhi Ye
Affiliations
Yingxuan Xu
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Shifeng Wang
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Yongcan Zhou
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Zhenyu Xie
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Bei Wang
Provincial Key Laboratory of Aquatic Animal Disease Control and Healthy Culture, College of Fishery, Guangdong Ocean University, Zhanjiang 524088, China
Zhangding Zhao
Hainan Baolu Aquatic Products Technology Co., Ltd., Haikou 570208, China
Wenlong Cai
Department of Infectious Diseases and Public Health, Jockey Club College of Veterinary Medicine and Life Sciences, City University of Hong Kong, Kowloon Tong, Hong Kong SAR, China
Peibo Wang
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Weiliang Guo
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Dongdong Zhang
Hainan Provincial Key Laboratory for Tropical Hydrobiology and Biotechnology, School of Marine Biology and Fisheries, Collaborative Innovation Center of Marine Science and Technology, School of Breeding and Multiplication (Sanya Institute of Breeding and Multiplication), Hainan University, Haikou 570228/Sanya 572025, China
Zhi Ye
MOE Key Laboratory of Marine Genetics and Breeding, College of Marine Life Sciences Ocean University of China, Qingdao 266071, China
Flavobacterium davisii is one of the causative agents of columnaris disease, significantly impacting Nile tilapia aquaculture. This study examines the invasion and immune evasion mechanisms of a highly virulent F. davisii strain through transcriptomic profiling of tilapia gills following acute immersion. We identified 8192 differentially expressed genes (DEGs) at 2 h, 6 h, and 12 h post-infection. They are enriched in pathways related to oxidative stress, immune suppression, tissue necrosis, and bacterial infection. Notably, early overexpression of rhamnose-binding lectin and mucin genes facilitated bacterial adhesion. Key immune genes, including those encoding major histocompatibility complex (MHC), immunoglobulins (Ig), Toll-like receptors (TLRs), and chemokines, were downregulated, indicating immune suppression. Conversely, immune evasion genes such as Fc receptor-like (FcRL) and programmed death-ligand 1 (PDL1) were upregulated, along with genes associated with reactive oxygen species (ROS) production, leading to increased tissue damage. Additionally, the upregulation of fibroblast growth factor and collagen genes suggested active tissue repair. In conclusion, F. davisii rapidly invades its host by enhancing adhesion to gill tissues, suppressing immune function, and inducing tissue damage. These findings enhance our understanding of F. davisii infection mechanisms and support the future breeding of disease-resistant tilapia and the development of sustainable control strategies.
