Hydrogen sulfide (HS) is a typical odour compound mainly causing respiratory and central nervous system symptoms. However, the immunotoxicity of inhaled HS and the underlying mechanisms remain largely unknown. In this study, a low-dose inhalation exposure to HS was arranged to observe inflammatory response and immunotoxicity in lung tissue of rats. Low concentrations of HS 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, HS 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.

中文翻译：

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长期吸入低浓度H2S引起大鼠肺组织免疫毒性和炎症反应

硫化氢（HS）是一种典型的气味化合物，主要引起呼吸道和中枢神经系统症状。然而，吸入HS的免疫毒性及其潜在机制仍然很大程度上未知。本研究通过低剂量吸入HS，观察大鼠肺组织的炎症反应和免疫毒性。低浓度H2S暴露影响肺组织和外周血的免疫水平。暴露组肺组织出现明显病理变化。在低浓度下，HS不仅诱导AQP-4和MMP-9表达上调，而且刺激免疫反应，启动各种抗炎和炎症因子，改变组织稳态环境。 TNF和趋化因子信号通路发挥了重要作用，可促进肺部炎症过程恶化并导致肺损伤和纤维化。过度的免疫反应会导致炎症反应和血气屏障损伤。这些数据对于评估未来的职业健康风险，为进一步开发可靠、灵敏、易用的接触伤害筛查指标提供技术支撑。