Hydrogen sulfide inhalation-induced immune damage is involved in oxidative stress, inflammation, apoptosis and the Th1/Th2 imbalance in broiler bursa of Fabricius

Abstract

Hydrogen sulfide (H₂S) is widely accepted to be a signaling molecule that exhibits some potentially beneficial therapeutic effects at physiological concentrations. At elevated levels, H₂S is highly toxic and has a negative effect on human health and animal welfare. Studies have shown that H₂S exposure induces an immune function in mice, but there are few studies of the effect of continuous H₂S exposure on immune organs in poultry. In this study, one-day-old broilers were selected and exposed to 4 or 20 ppm of H₂S gas for 14, 28 and 42 days of age. After exposure, the bursa of Fabricius (BF) was harvested. The results showed that continuous H₂S exposure reduced the body weight, abdominal fat percentage, and antibody titer in broilers. H₂S exposure also decreased mRNA expression of IgA, IgM and IgG in the broiler BF. A histological study revealed obvious nuclear debris, and a few vacuoles in the BF, and an ultrastructural study revealed mitochondrial and nuclear damage to BF cells after H₂S exposure for 42 d. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay suggested H₂S exposure remarkably increased the number of TUNEL positive nuclei and significantly increased apoptotic index. The expression of apoptotic genes also confirmed that H₂S inhalation damaged the broiler BF. Increased cytokines and reduced antioxidant responses were detected in the BF after exposure to H₂S. Cytokines promoted inflammation and caused a Th1/Th2 imbalance. We suggest that continuous H₂S intoxication triggers oxidative stress, inflammation, apoptosis and a Th1/Th2 imbalance in the BF, leading to immune injury in broilers.

Keywords: Apoptosis; Broiler; Cytokines; Hydrogen sulfide; Immune injury; Oxidative stress.