The immune responses of the Chinese rare minnow (Gobiocypris rarus) exposed to environmentally relevant concentrations of cypermethrin and subsequently infected by the bacteria Pseudomonas fluorescens.

In the present study, to assess the immunotoxicity of cypermethrin (CYP) in fish, Chinese rare minnows (Gobiocypris rarus) were exposed to environmentally relevant concentrations (0.15, 0.5, and 1.5 μg/L) of CYP for 28 d and subjected to pathogen challenge trials for 2 d. After 28 d of CYP exposure, the levels of Immunoglobulin M (IgM), Alkaline phosphatase (ALP), and C-reactive protein (CRP) were significantly decreased (p < 0.05) after treatment with 1.5 μg/L CYP. Moreover, an induction of inflammatory cytokine transcripts (tnfa, il-6, il-8, and il-12) was observed (p < 0.05) after treatment with 1.5 μg/L CYP. After challenge with Pseudomonas fluorescens (P. fluorescens), plasma lysozyme (LYS) activity at 24 and 48 hours post-injection (hpi) was significantly decreased in the 0.5 and 1.5 μg/L CYP treatment groups (p < 0.05). Moreover, liver Complement component 3 (C3) and CRP contents at 24 hpi were significantly decreased in the 1.5 μg/L CYP treatment group (p < 0.05), whereas significant decreases in liver C3 and IgM contents were observed at 48 hpi (p < 0.05). Inhibition of expression of Toll-like receptor-nuclear factor kappa B (TLR-NF-kB) signaling pathway-related genes was observed in the CYP treatment groups and resulted in significant down-regulation of inflammatory cytokines (il-1β and il-12) in the 1.5 μg/L CYP treatment group at 48 hpi (p < 0.05). Interestingly, the mortality in the 0.5 and 1.5 μg/L CYP treatments was significantly increased at 48 hpi (p < 0.05). These results indicated that environmentally relevant concentrations of CYP suppressed the Chinese rare minnow immune system and reduced immune defense against bacterial infection, thereby causing subsequent mortality. Meanwhile, our results demonstrated that a subsequent host resistance challenge is an effective method for determining the immunotoxicity of chemicals (e.g., CYP).