A vast range of research related to the heavy metal cadmium (Cd) toxicity has been carried out in a wide variety of fish species. However, Cd induced immunomodulation in monocytes/macrophages of Channa punctatus Bloch. has rarely been explored. The present study was designed to determine Cd induced immune response, role of NF-κB (Nuclear factor kappa B) pathway and the subsequent downstream molecular responses in monocytes/macrophages of C. punctatus. Fish were sampled and acclimatized, with one group treated with cadmium chloride (CdCl₂) (1.96 mg/L) and another kept as untreated control group, both under observation for 7 days. Exposure to CdCl₂ was found to alter hematological profile of C. punctatus in addition to incurring histo-architectural damages in the HK (head kidney) and ultrastructural changes in the monocytes/macrophages. The innate immune potential was found to be significantly compromised as evident from decreased phagocytosis, intracellular killing, cell adhesion and reduced release of nitric oxide (NO) and myeloperoxidase (MPO) in Cd intoxicated group. Also Cd triggered ROS generation, reduced cellular NO levels by forming peroxynitrite along with the upregulated expression of inflammatory marker iNOS (inducible nitric oxide synthase) in monocyte/macrophages, both at mRNA and protein levels, indicating inflammation. Inflammation is further verified from the upregulated expression of proinflammatory cytokines viz. TNF-α, IL-1β, IL-6, IL-12 along with a central inflammatory mediator NF-κΒ and downregulation of the anti-inflammatory cytokine IL-10, both at mRNA and protein level. It can be concluded that, a sub-lethal exposure of Cd in C. punctatus for 7 days caused significant alterations in the hematological, histological and ultrastructural profile in monocyte/macrophages; impaired innate immune parameters, triggers ROS generation and inflammation as validated from the upregulated expression of NF-κΒ, iNOS, TNF-α, IL-1β, IL-6, IL-12 and IL-10 down regulation.

在各种鱼类中都进行了与重金属镉（Cd）毒性有关的大量研究。但是，Cd会诱导马鞭草（Channa punctatus Bloch）单核细胞/巨噬细胞中的免疫调节。很少被探索。本研究旨在确定Cd诱导的免疫应答，NF-κB（核因子κB）途径的作用以及随后的点状梭菌单核细胞/巨噬细胞下游分子应答。对鱼取样并使其适应环境，其中一组用氯化镉（CdCl ₂）（1.96 mg / L）处理，另一组作为未处理的对照组，均观察7天。暴露于氯化镉₂被发现改变的血液学轮廓C.毛虫除了在HK（头部肾脏）中引起组织结构损伤和单核细胞/巨噬细胞的超微结构变化外。镉中毒组吞噬作用降低，细胞内杀伤，细胞粘附和一氧化氮（NO）和髓过氧化物酶（MPO）释放减少，证明其固有的免疫潜能受到显着损害。镉还触发ROS的产生，通过形成过氧亚硝酸盐以及炎症标记iNOS（诱导型一氧化氮合酶）在单核细胞/巨噬细胞中的mRNA和蛋白质水平的表达上调而降低了细胞的NO水平。从促炎细胞因子即上调表达进一步证实了炎症。TNF-α，IL-1β，IL-6，IL-12与中枢炎性介质NF-κB以及抗炎细胞因子IL-10的下调（在mRNA和蛋白质水平上）。可以得出结论，镉的亚致死性暴露于连续7天的马尾藻导致单核细胞/巨噬细胞的血液学，组织学和超微结构的显着改变；NF-κB，iNOS，TNF-α，IL-1β，IL-6，IL-12和IL-10的下调可证明先天免疫参数受损，触发ROS生成和炎症。