Regulating of LncRNA2264/miR-20b-5p/IL17RD axis on hydrogen sulfide exposure-induced inflammation in broiler thymus by activating MYD88/NF-κB pathway. (15th February 2022)

• Record Type: Journal Article
• Authors: Wang, Yu; He, Yujiao; Hu, Xueyuan; Chi, Qianru; Zhao, Bing; Ye, Jingying; Li, Shu
• Is Part Of: Toxicology. Volume 467(2022)
• Publication Date: 2022-02-15
• Subjects: H2S -- ncRNA -- IL17RD -- Chicken -- Thymus -- Inflammation; Toxicology -- Periodicals; Chemicals -- Physiological effect -- Periodicals; 615.9005
• DOI: 10.1016/j.tox.2021.153086
• Languages: English
• ISSNs: 0300-483X

Abstract

Graphical abstract: Highlights: H2 S induces inflammation in broiler thymus. H2 S exposure causes changes in the lncRNA profiles of broiler thymus. LncRNA2264 acts as the sponge of miR-20b-5p to negative regulate IL17RD. LncRNA2264/miR-20b-5p/IL17RD aixs is involved in thymus injury caused by H2 S. Down-regulating IL17RD contributes to the activation of the MYD88/NF-κB pathway. Abstract: Hydrogen sulfide (H2 S) is an environmental pollutant. Chronic exposure to H2 S can damage the immune system of birds, but the detailed mechanisms of H2 S-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 H2 S-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 H2 S-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 H2 S-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 H2 S 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. H2 S 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 H2 S exposure-induced thymic inflammation, which has positive implications for guiding the prevention and control of H2 S gas poisoning in livestock housing and ensuring animal welfare.