Yang Yanjian, Zhang Guanrong, Xu Ruilong, Deng Yiyang, Mo Zequan, Li Yanwei, Dan Xueming
Nansha-South China Agricultural University Fishery Research Institute, Guangzhou 511457, China.
University Joint Laboratory of Guangdong Province, Hong Kong and Macao Region on Marine Bioresource Conservation and Exploitation, Guangdong Laboratory for Lingnan Modern Agriculture, College of Marine Sciences, South China Agricultural University, Guangzhou 510642, China.
Biology (Basel). 2025 Aug 2;14(8):986. doi: 10.3390/biology14080986.
() is a globally significant aquatic pathogen responsible for severe economic losses in aquaculture. While the infection often exhibits distinct seasonal patterns strongly correlated with water temperature, there is limited knowledge regarding the temperature-dependent immune evasion strategies of . Our results demonstrated a striking temperature-dependent virulence phenotype, with significantly higher mortality rates observed at high temperature (HT, 33 °C) compared to low temperature (LT, 23 °C). Proteomic analysis revealed temperature-dependent upregulation of key virulence factors, including streptolysin S-related proteins (SagG, SagH), antioxidant-related proteins (SodA), and multiple capsular polysaccharide (cps) synthesis proteins (cpsD, cpsH, cpsL, cpsY). Flow cytometry analysis showed that HT infection significantly reduced the percentage of lymphocyte and myeloid cell populations in the head kidney leukocytes of , which was associated with elevated expression and increased apoptosis. In addition, HT infection significantly inhibited the release of reactive oxygen species (ROS) but not nitric oxide (NO) production. Using cps-deficient mutant, Δcps, we demonstrated that the cps is essential for temperature-dependent phagocytosis resistance in , as phagocytic activity against Δcps remained unchanged across temperatures, while NS-1 showed significantly reduced uptake at HT. These findings provide new insights into the immune evasion of under thermal regulation, deepening our understanding of the thermal adaptation of aquatic bacterial pathogens.
（某病原体）是一种在全球范围内具有重要影响的水生病原体，会给水产养殖带来严重经济损失。虽然该病原体感染通常呈现出与水温密切相关的明显季节性模式，但关于其温度依赖性免疫逃避策略的了解却很有限。我们的研究结果显示出一种显著的温度依赖性毒力表型，与低温（LT，23℃）相比，在高温（HT，33℃）下观察到的死亡率显著更高。蛋白质组学分析揭示了关键毒力因子的温度依赖性上调，包括链球菌溶血素S相关蛋白（SagG、SagH）、抗氧化相关蛋白（SodA）以及多种荚膜多糖（cps）合成蛋白（cpsD、cpsH、cpsL、cpsY）。流式细胞术分析表明，HT感染显著降低了该病原体头肾白细胞中淋巴细胞和髓样细胞群体的百分比，这与该病原体表达升高和细胞凋亡增加有关。此外，HT感染显著抑制了活性氧（ROS）的释放，但不影响一氧化氮（NO）的产生。使用该病原体的cps缺陷突变体Δcps，我们证明了cps对于该病原体温度依赖性吞噬抗性至关重要，因为在不同温度下对Δcps的吞噬活性保持不变，而NS - 1在HT时摄取显著减少。这些发现为热调节下该病原体的免疫逃避提供了新见解，加深了我们对水生细菌病原体热适应性的理解。
