PUBLICATION
Zebrafish nos2a benefits bacterial proliferation via suppressing ROS and inducing NO production to impair the expressions of inflammatory cytokines and antibacterial genes
- Authors
- Zheng, S.Y., Shao, X., Qi, Z., Yan, M., Tao, M.H., Wu, X.M., Zhang, L., Ma, J., Li, A., Chang, M.X.
- ID
- ZDB-PUB-231021-55
- Date
- 2023
- Source
- Fish & shellfish immunology 142: 109178 (Journal)
- Registered Authors
- Keywords
- Edwardsiella piscicida infection, Nitric oxide, ROS, Zebrafish, nos2a
- MeSH Terms
-
- Animals
- Cell Proliferation
- Cytokines
- Edwardsiella*/physiology
- Enterobacteriaceae Infections*
- Mammals/metabolism
- Nitric Oxide/metabolism
- Nitric Oxide Synthase Type II/genetics
- Nitric Oxide Synthase Type II/metabolism
- Reactive Oxygen Species/metabolism
- Zebrafish
- PubMed
- 37863126 Full text @ Fish Shellfish Immunol.
Citation
Zheng, S.Y., Shao, X., Qi, Z., Yan, M., Tao, M.H., Wu, X.M., Zhang, L., Ma, J., Li, A., Chang, M.X. (2023) Zebrafish nos2a benefits bacterial proliferation via suppressing ROS and inducing NO production to impair the expressions of inflammatory cytokines and antibacterial genes. Fish & shellfish immunology. 142:109178.
Abstract
The enzyme nitric oxide synthase 2 or inducible NOS (NOS2), reactive oxygen species (ROS) and nitric oxide (NO) are important participants in various inflammatory and immune responses. However, the functional significances of the correlations among piscine NOS2, ROS and NO during pathogen infection remain unclear. In teleost, there are two nos2 genes (nos2a and nos2b). It has been previously reported that zebrafish nos2a behaves as a classical inducible NOS, and nos2b exerts some functions similar to mammalian NOS3. In the present study, we reported the functional characterization of zebrafish nos2a during bacterial infection. We found that zebrafish nos2a promoted bacterial proliferation, accompanied by an increased susceptibility to Edwardsiella piscicida infection. The nagative regulation of zebrafish nos2a during E. piscicida infection was characterized by the impaired ROS levels, the induced NO production and the decreased expressions of proinflammatory cytokines, antibacterial genes and oxidant factors. Furthermore, although both inducing ROS and inhibiting NO production significantly inhibited bacterial proliferation, only inhibiting NO production but not inducing ROS significantly increased resistance to E. piscicida infection. More importantly, ROS supplementation and inhibition of NO completely abolished this detrimental consequence mediated by zebrafish nos2a during E. piscicida infection. All together, these results firstly demonstrate that the innate response mediated by zebrafish nos2a in promoting bacterial proliferation is dependent on the lower ROS level and higher NO production. The present study also reveals that inhibition of NO can be effective in the protection against E. piscicida infection.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping