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Ammonia (NH3) is a toxic, environmental pollutant, and irritant gas. Previous studies reported the toxic effects of NH3 which led to inflammation in various organs of chicken. However, the exact mechanism of NH3-induced inflammation in chicken lymphoid organs bursa of fabricius (BF) and thymus is still elusive. Thus, this study was designed to investigate NH3-induced inflammation in chicken BF and thymus. Experimental chickens were divided into low (5.0 mg/m3), middle (10.0–15.0 mg/m3), and high (20.0–45.0 mg/m3) NH3-treated groups. To investigate NH3-induced inflammation in chicken's BF and thymus, histological observation, NO content and iNOS activity, inflammatory cytokine contents, and mRNA levels were performed by light microscopy, microplate spectrophotometer, ELISA assay, and qRT-PCR. The finding of the present study showed that NH3 exposure reduced BF and thymus index, increased nitric oxide (NO) content and inducible nitric oxide synthase (iNOS) activity, inflammatory cytokine contents and mRNA levels of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (Cox-2), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-10, IL-1β, IL-18, toll-like receptor 2A (TLR-2A), and iNOS. Histopathological examination revealed signs of inflammation including increased nuclear debris and vacuoles in the cortex and medulla of thymus and bursal follicles. Conclusively, our findings displayed that NH3 exposure affects the normal function of BF and thymus and led inflammation. The data provided a new ground for NH3-induced toxicity and risk assessment in chicken production. [ABSTRACT FROM AUTHOR]

Ammonia (NH 3) is considered as environmental pollutant and toxic agent for animals and humans including poultry. Previous reports demonstrated that NH 3 suppressed broilers immunity. However, the harmful effects of NH 3 on broilers bursa of fabricius (BF) is still unknown. Functionally, apoptosis is very important for many physiological processes including homeostasis of lymphocyte population. Therefore, the present study was aimed to investigate the underlying mechanisms of NH 3 toxicity in the broilers BF. Histological observation showed lymphocyte accumulation, cavities and increased interstitial cells in BF. Ultrastructural observation indicated mitochondrial vacuoles, deformation and disappearance of mitochondrial membranes. Oxidative stress markers (CAT, MDA, H 2 O 2 , GGT, GSH-Px and GSH) showed that NH 3 -induced oxidative stress in BF. Meanwhile, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay revealed increased apoptotic cells. In addition, the mRNA and protein expression of dynamin-related protein 1 (Drp1), mitochondrial fission factor (Mff), mitofusin 1 and 2 (Mfn1 and Mfn2), optic atrophy 1 (Opa1) indicated imbalance between mitochondrial inner and outer membrane and results in mitochondrial dysfunction in broilers BF. The mRNA and protein expression of apoptosis-related genes including Caspase-3, Caspase-9, Caspase-8, Cytochrome-C (Cyt-C), p53, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were significantly altered in broilers BF. Conclusively, these results displayed that excessive NH 3 causes BF damage and mitochondrial dysfunction through oxidative stress and apoptosis in BF and could affect immune function of BF. These findings provide possible therapeutic targets to prevent NH 3 induced toxicity in the BF of broilers. • The effects of ammonia (NH 3)-induced toxicity in broilers BF were investigated. • NH 3 -induced abnormal morphological and ultrastructural changes in the BF of broilers. • NH 3 inhalation causes a significant increase in oxidative stress and induced apoptosis. • The study provide possible therapeutic targets to prevent NH 3 -induced immune toxicity. [ABSTRACT FROM AUTHOR]