Hydrogen sulfide (H2S), the gaseous mediator produced by various cells in our body, was recently discovered to play a major role in human physiology despite its toxic nature known for centuries. In addition to its pathophysiological relevance in cardiovascular and neuronal disorders, there is considerable interest in the significance of H2S in inflammation. A number of preclinical studies in our laboratory as well as by others, using H2S donors and inhibitors of its endogenous synthesis, have provided evidence for both pro- and anti-inflammatory character of H2S. But so far, there is a significant lack of support from relevant clinical studies. One of the major contentious issues being variable dose and sampling time, controversies exist on the precise friend or foe nature of this gaseous transmitter. However, it is well accepted that once a clearer picture of the whole story of H2S in inflammation emerges, potential for therapeutic manipulations in this field are immense. This review focuses on the intriguing effects of H2S in some of the inflammatory conditions such as acute pancreatitis, sepsis, burn injuries and local inflammation of the joints. Active research projects have been undertaken to elucidate the mechanisms of action of H2S in inflammation, including neurogenic inflammation and interaction with other biological mediators and pathways. The early and fragmentary evidence obtained holds promise for a successful drug intervention for these inflammatory diseases.
Keywords: Acute pancreatitis, burn, hydrogen sulfide, inflammation, sepsis, substance P, neurogenic inflammation, lipopolysaccharide (LPS)-induced endotoxemia, cecal ligation and puncture (CLP)-induced sepsis, extracellular signal-regulated kinase, NF-κB
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