[11] Furthermore, H2S inhibits neutrophil adhesion and activation in response to inflammatory stimuli and suppresses the release of the pro-inflammatory mediator tumor necrosis factor-alpha. [34], [35] Other studies report that H2S mediates pro-inflammatory effects by potentiating sulfide production in neutrophils [36] and mediating leukocyte activation. [37] Although granulocyte influx seems to be reduced by treatment with H2S, literature is inconclusive on the contribution of neutrophil invasion to final myocardial infarct size and appears not to be a dominant factor [38]. This evidence concerns the gene TNF and myocardial infarction.