The imbalance of Th1/Th2 triggers an inflammatory response in chicken spleens after ammonia exposure

Graphical abstract

Abstract

Ammonia is a hazardous environmental pollutant that can be harmful to animal health. In this study, we aimed to evaluate the effect of ammonia exposure on broiler chicken spleens. We randomly divided one hundred twenty 1-day-old broiler chickens into 3 groups and raised them with exposure to different ammonia concentrations (low, middle, and high); at 42 D of age, the chicken spleens were extracted. We observed histopathologic changes in spleen tissues by microscopy and measured the expression of Th1/Th2 secreted cytokines (interleukin [ IL]-1β, IL-2, IL-4, IL-6, IL-10, interferon-γ [ IFN - γ], tumor necrosis factor-α) by RT-PCR. We also measured the expression of nuclear receptor-κB ( NF- κ B) pathway–related genes (cyclooxygenase-2 [ COX-2], nitric oxide synthase [ iNOS], and prostaglandin synthetase [ PGE]) in spleens by RT-PCR and Western blot analysis. Histopathologic observations indicated that the spleen tissues were seriously injured in the high ammonia concentration group. There was abnormal cytokine expression, including increased IL-4, IL-6, and IFN-γ and decreased IL-2, which indicated an imbalance in the Th1/Th2 response. The proinflammatory factors such as NF-κB, COX-2, iNOS, and PGE were upregulated in the high ammonia group. In conclusion, this study illustrated that ammonia exposure led to a Th1/Th2 immune imbalance and triggered the NF-κB pathway, causing inflammatory damage to the spleen.