The gills of the common carp, whose mucosal surface belongs to the key defence mechanisms of piscine immunity, can be infested with both the larval and adult stage of Eudiplozoon nipponicum (Monogenea). Although on their own, monogeneans do not considerably compromise their hosts’ health status, fish with epithelial barriers damaged in parasite feeding and attachment sites are at an increased risk of bacterial challenge with possible harmful consequences. Several studies suggest that helminth parasites of teleost fish evade and manipulate host immune system via their excretory-secretory products, but our knowledge of these processes in the monogeneans is limited. Cysteine peptidase inhibitors (CPI), which are found in the secretions of numerous parasites, often induce immunosuppression by subverting Th1 mechanisms and drawing the immune system towards a Th2/Treg response. We employed the qPCR to test the effect of recently characterised CPI of E. nipponicum (rEnStef) on the mRNA expression of pro-inflammatory cytokine TNF-α and anti-inflammatory cytokine IL-10 produced by porcine macrophages in vitro. After an initial preincubation with rEnStef, we stimulated the macrophages using LPS. By inducing a Th1 pro-inflammatory response, we imitated the immune reaction during a bacterial challenge in tissue damaged by the feeding and attachment of E. nipponicum. We observed a significant dose-dependent downregulation of the expression of TNF-α and IL-10 cytokines. The observed suppression of TNF-alpha expression by rEnStef could result in decreased pathogen control, which might in turn lead to increased rates of secondary bacterial infections in fish infected by E. nipponicum.

鲤鱼的粘膜表面属于鱼类免疫力的关键防御机制，其can可能同时被幼虫和成年大戟鱼（Eudiplozoon nipponicum（Monogenea））感染。尽管单基因动物本身并不会严重损害其寄主的健康状况，但在寄生虫摄食和附着位点上皮屏障被破坏的鱼类面临细菌攻击的风险增加，可能带来有害后果。多项研究表明，硬骨鱼类的蠕虫寄生虫可通过以下途径逃避和操纵宿主的免疫系统他们的排泄分泌产品，但是我们对单基因的这些过程的了解是有限的。在许多寄生虫的分泌物中发现的半胱氨酸肽酶抑制剂（CPI）通常通过破坏Th1机制并使免疫系统趋向Th2 / Treg反应来诱导免疫抑制。我们所采用的定量PCR来测试的最近表征CPI的效果E. nipponicum（rEnStef）对猪巨噬细胞产生促炎症细胞因子TNF-α和抗炎性细胞因子IL-10的mRNA表达在体外。在与rEnStef进行初步预孵育后，我们使用LPS刺激了巨噬细胞。通过诱导Th1促炎反应，我们在细菌攻击过程中模仿了细菌攻击过程中的免疫反应，该组织受饲喂和附着的损害E. nipponicum。我们观察到TNF-α和IL-10细胞因子表达的显着剂量依赖性下调。观察到的rEnStef对TNF-α表达的抑制作用可能导致病原体控制力降低，这反过来可能导致被E. nipponicum感染的鱼类继发细菌感染的比率增加。