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| Main Authors: | , , , , , , , , , , |
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| Format: | Artículo científico |
| Language: | en |
| Published: |
Biology
2024
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| Online Access: | https://pubmed.ncbi.nlm.nih.gov/39596849/ |
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| _version_ | 1868266275378036736 |
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| author | Xu, Yingxuan Wang, Shifeng Zhou, Yongcan Xie, Zhenyu Wang, Bei Zhao, Zhangding Cai, Wenlong Wang, Peibo Guo, Weiliang Zhang, Dongdong Ye, Zhi |
| author_facet | Xu, Yingxuan Wang, Shifeng Zhou, Yongcan Xie, Zhenyu Wang, Bei Zhao, Zhangding Cai, Wenlong Wang, Peibo Guo, Weiliang Zhang, Dongdong Ye, Zhi Xu, Yingxuan Wang, Shifeng Zhou, Yongcan Xie, Zhenyu Wang, Bei Zhao, Zhangding Cai, Wenlong Wang, Peibo Guo, Weiliang Zhang, Dongdong Ye, Zhi |
| collection | PubMed - marine biology |
| contents | Immune Suppression and Rapid Invasion of Nile Tilapia Gills Following an Acute Challenge by . Xu, Yingxuan Wang, Shifeng Zhou, Yongcan Xie, Zhenyu Wang, Bei Zhao, Zhangding Cai, Wenlong Wang, Peibo Guo, Weiliang Zhang, Dongdong Ye, Zhi 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 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, rapidly invades its host by enhancing adhesion to gill tissues, suppressing immune function, and inducing tissue damage. These findings enhance our understanding of infection mechanisms and support the future breeding of disease-resistant tilapia and the development of sustainable control strategies. |
| format | Artículo científico |
| id | pubmed_39596849 |
| institution | PubMed |
| language | en |
| publishDate | 2024 |
| publisher | Biology |
| record_format | pubmed |
| spellingShingle | Immune Suppression and Rapid Invasion of Nile Tilapia Gills Following an Acute Challenge by . Xu, Yingxuan Wang, Shifeng Zhou, Yongcan Xie, Zhenyu Wang, Bei Zhao, Zhangding Cai, Wenlong Wang, Peibo Guo, Weiliang Zhang, Dongdong Ye, Zhi Immune Suppression and Rapid Invasion of Nile Tilapia Gills Following an Acute Challenge by . Xu, Yingxuan Wang, Shifeng Zhou, Yongcan Xie, Zhenyu Wang, Bei Zhao, Zhangding Cai, Wenlong Wang, Peibo Guo, Weiliang Zhang, Dongdong Ye, Zhi 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 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, rapidly invades its host by enhancing adhesion to gill tissues, suppressing immune function, and inducing tissue damage. These findings enhance our understanding of infection mechanisms and support the future breeding of disease-resistant tilapia and the development of sustainable control strategies. |
| title | Immune Suppression and Rapid Invasion of Nile Tilapia Gills Following an Acute Challenge by . |
| url | https://pubmed.ncbi.nlm.nih.gov/39596849/ |