Division of Fish Health, University of Veterinary Medicine, Vienna, Austria.
VetCore, University of Veterinary Medicine, Vienna, Austria.
Front Cell Infect Microbiol. 2024 May 13;14:1369615. doi: 10.3389/fcimb.2024.1369615. eCollection 2024.
Little is known about the proteomic changes at the portals of entry in rainbow trout after infection with the myxozoan parasites, , and . Whirling disease (WD) is a severe disease of salmonids, caused by the myxosporean , while, proliferative kidney disease (PKD) is caused by , which instead belongs to the class Malacosporea. Climate change is providing more suitable conditions for myxozoan parasites lifecycle, posing a high risk to salmonid aquaculture and contributing to the decline of wild trout populations in North America and Europe. Therefore, the aim of this study was to provide the first proteomic profiles of the host in the search for evasion strategies during single and coinfection with and .
One group of fish was initially infected with and another group with . After 30 days, half of the fish in each group were co-infected with the other parasite. Using a quantitative proteomic approach, we investigated proteomic changes in the caudal fins and gills of rainbow trout before and after co-infection.
In the caudal fins, 16 proteins were differentially regulated post exposure to , whereas 27 proteins were differentially modulated in the gills of the infected rainbow trout post exposure to . After co-infection, 4 proteins involved in parasite recognition and the regulation of host immune responses were differentially modulated between the groups in the caudal fin. In the gills, 11 proteins involved in parasite recognition and host immunity, including 4 myxozoan proteins predicted to be virulence factors, were differentially modulated.
The results of this study increase our knowledge on rainbow trout co-infections by myxozoan parasites and rainbow trout immune responses against myxozoans at the portals of entry, supporting a better understanding of these host-parasite interactions.
目前对于感染粘孢子虫寄生虫 、 和 后虹鳟鱼进入门户的蛋白质组变化知之甚少。旋毛虫病（WD）是鲑鱼的一种严重疾病，由粘孢子虫引起，而增殖性肾病（PKD）是由 引起的，它属于粘体动物门 Malacosporea 类。气候变化为粘孢子虫寄生虫的生命周期提供了更适宜的条件，对鲑鱼养殖业构成了高风险，并导致北美和欧洲野生鳟鱼数量减少。因此，本研究的目的是提供宿主的蛋白质组图谱，以寻找在单一和混合感染 和 时的逃避策略。
一组鱼最初感染了 和 ，另一组鱼感染了 。30 天后，每组鱼的一半进行混合感染。我们采用定量蛋白质组学方法，研究了虹鳟鱼在混合感染前后尾鳍和鳃中的蛋白质组变化。
在尾鳍中，有 16 种蛋白质在暴露于 后发生差异调节，而在感染虹鳟鱼的鳃中，有 27 种蛋白质在暴露于 后发生差异调节。混合感染后，在尾鳍中，有 4 种与寄生虫识别和宿主免疫反应调节有关的蛋白质在两组之间发生差异调节。在鳃中，有 11 种与寄生虫识别和宿主免疫有关的蛋白质发生差异调节，包括 4 种被预测为毒力因子的粘孢子虫蛋白。
本研究的结果增加了我们对虹鳟鱼感染粘孢子虫寄生虫和虹鳟鱼对进入门户的粘孢子虫的免疫反应的了解，有助于更好地理解这些宿主-寄生虫相互作用。
