Abstract
Accumulating evidence has suggested that hydrogen sulfide (H2S) naturally occurs during cysteine metabolism in many types of mammalian cells. Since H2S exhibits vasodilator activity and plays an important role in nervous system and inflammatory diseases, it is currently considered to be the third gaseous mediator. Recently, more and more attention has been paid to the biological functions of H2S in acute lung injury (ALI) and/or acute respiratory distress syndrome (ARDS). In various animal models of lung injury, H2S has been demonstrated to contribute to the development and progression of lung inflammation and injury. Regulating the endogenous level of H2S is possible to protect animals against lung injury. H2S may exert its effect on ALI/ARDS by modulating leukocyte activation. In addition, H2S may induce lung inflammation and injury via activating sensory nerves in lung and eliciting a neurogenic inflammatory response.