Chronic inhalation of H2S in low concentration induces immunotoxicity and inflammatory effects in lung tissue of rats

• Published in: Ecotoxicology and environmental safety Vol. 276; p. 116279
• Main Authors: Li, Kexian, Wang, Jian, Fang, Liben, Lou, Yinghua, Li, Jue, Li, Qihui, Luo, Qun, Zheng, Xiaowei, Fang, Jingjing
• Format: Journal Article
• Language: English
• Published: Elsevier Inc 01.05.2024; Elsevier
• Subjects: Hydrogen sulfide; Immunotoxicity; Inflammatory response; Lung tissue; Signaling pathway; Hydrogen sulfide; Inflammatory response; Signaling pathway; Lung tissue; Immunotoxicity
• ISSN: 0147-6513; 1090-2414
• DOI: 10.1016/j.ecoenv.2024.116279

Hydrogen sulfide (H2S) is a typical odour compound mainly causing respiratory and central nervous system symptoms. However, the immunotoxicity of inhaled H2S and the underlying mechanisms remain largely unknown. In this study, a low-dose inhalation exposure to H2S was arranged to observe inflammatory response and immunotoxicity in lung tissue of rats. Low concentrations of H2S exposure affected the immune level of pulmonary tissue and peripheral blood. Significant pathological changes in lung tissue in the exposure group were observed. At low concentration, H2S not only induced the upregulation of AQP-4 and MMP-9 expression but also stimulated immune responses, initiating various anti-inflammatory and inflammatory factors, altering tissue homeostatic environments. The TNF and chemokine signaling pathway played an important role which can promote the deterioration of pulmonary inflammatory processes and lead to lung injury and fibrosis. Excessive immune response causes an inflammatory effect and blood-gas barrier damage. These data will be of value in evaluating future occupational health risks and providing technical support for the further development of reliable, sensitive, and easy-to-use screening indicators of exposure injury. [Display omitted] •H2S Induces Immunotoxicity and Inflammatory Effects.•Apoptosis, immune activity of alveolar macrophages, inflammatory cell infiltration and alveoli wall thickening were observed.•AQP-4 and MMP-9 in lung tissue up-regulated.•IL-1α, IL-1β, Marco, TNF-α and CC16 gene un-regulated and Bcl3 and Cflar down-regulated.•H2S exposure triggered the complex immune response in lung through chemokine pathway and TNF pathway.