Research ArticleInflammation

Depletion of H2S during obesity enhances store-operated Ca2+ entry in adipose tissue macrophages to increase cytokine production

See allHide authors and affiliations

Science Signaling  15 Dec 2015:
Vol. 8, Issue 407, pp. ra128
DOI: 10.1126/scisignal.aac7135

Limiting inflammation in obesity

Obese individuals have increased amounts of inflammatory cytokines in the circulation, which are produced by adipose tissue macrophages (ATMs). Velmurugan et al. found that ATMs from obese mice had decreased amounts of the gaseous signaling molecule hydrogen sulfide (H2S) than did ATMs from lean mice. ATMs from obese mice had enhanced store-operated calcium entry and produced more proinflammatory cytokines. Treatment of macrophages with the bacterial product lipopolysaccharide also decreased H2S concentrations and increased inflammatory cytokine production. Knockdown experiments showed that H2S inhibited the channel protein Orai3 to reduce calcium entry into macrophages. Together, these data suggest that inflammatory stimuli lead to the depletion of H2S in adipose tissue, which exacerbates inflammatory responses by resident ATMs.