Arsenic (III) or/and copper (II) exposure induce immunotoxicity through trigger oxidative stress, inflammation and immune imbalance in the bursa of chicken.

The environmental hazards of arsenic (As) and copper (Cu) contamination have swept through quite a few districts worldwide. Whereas, molecular mechanisms involved in As- and Cu-induced immunotoxicity in Gallus gallus bursa of Fabricius (BF) are complex and elusive. Male Hy-line chickens were exposed to arsenic trioxide (AsO; 30 mg/kg) and copper sulfate (CuSO; 300 mg/kg) alone or in combination, respectively, to examine the potential ecotoxicity of them. The ions homeostasis and BF index of chicken had distinct changes after As or/and Cu exposure. Moreover, As or/and Cu treatment significantly increased the MDA content and NOS activity, and simultaneously resulted in reductions in CAT and AHR activities. Subsequently, it was further exhibited up-regulations of nuclear factor-κB (NF-κB), inflammatory mediators and pro-inflammation cytokines accompanied by depletion of anti-inflammatory cytokines and severe pathological conditions. Moreover, decreased ratio of IFN-γ/IL-4 and increased level of IL-17 illustrated an imbalance of the immune response. Meanwhile, incremental mRNA transcription and protein levels of heat shock proteins (HSPs) alleviated toxicity caused by As or/and Cu. Importantly, exposure to both contaminants significantly soared the BF injury in comparison with exposure to As or Cu alone. All these results illustrated that exposure to AsO or/and CuSO elicited BF tissue damage and ions changes, and its severity was associated with prolonged persistence of oxidative damage, accompanied by a dysregulated immune response which played a vital role in inflammatory injury. Additionally, combined management of AsO and CuSO could exacerbate BF injury.