Regulating of LncRNA2264/miR-20b-5p/IL17RD axis on hydrogen sulfide exposure-induced inflammation in broiler thymus...

Hydrogen sulfide (H₂S) is an environmental pollutant. Chronic exposure to H₂S can damage the immune system of birds, but the detailed mechanisms of H₂S-induced thymus toxicity have not been determined. Competitive endogenous RNA (ceRNA) mechanism participates in many pathophysiological processes by regulating gene expression, including environmental pollutant-induced injury. Therefore, we investigate the specific mechanisms of ceRNA in the process of H₂S-induced thymic immune damage in broiler chickens. In the current study, 120 one-day-old male Ross 308 broilers were randomly divided into two groups (n = 60 chickens/group), raising in the control chamber (0.5 ± 0.5 ppm) or H₂S-exposed chamber (4.0 ± 0.5 ppm at 0-3 weeks of age and 20.0 ± 0.5 ppm at 4-6 weeks of age groups) to replicate the H₂S-exposed broilers. NaHS (3 mM or 6 mM) was used to treat chicken macrophages (HD11) to establish an in vitro. Histopathology and ultrastructural changes of thymus were assessed by hematoxylin and eosin (H&E) staining and transmission electron microscopy (TEM). Gene expression profiles were analyzed by using transcriptomics. The underlying mechanisms of thymic injury were further revealed by dual luciferase reporter gene assay, qRT-PCR and Western blotting. Research results showed that H₂S exposure induced an inflammatory response in thymus, with the expression of LncRNA2264 was significantly down-regulated. LncRNA2264 could competitively bind to miR-20b-5p and caused downregulation of the IL17RD. H₂S could activate inflammatory factors through the LncRNA2264/miR-20b-5p/IL17RD axis. In summary, this study suggested that LncRNA2264 acted as a miR-20b-5p molecular sponge to regulate the expression of IL17RD involved in H₂S exposure-induced thymic inflammation, which has positive implications for guiding the prevention and control of H₂S gas poisoning in livestock housing and ensuring animal welfare.