Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Abstract

Hydrogen sulfide is rapidly gaining ground as a physiological mediator of inflammation, but there is no clear consensus as to its precise role in inflammatory signaling. This article discusses the disparate anti-inflammatory (‘the good’) and proinflammatory (‘the bad’) effects of endogenous and pharmacological H₂S in disparate animal model and cell culture systems. We also discuss ‘the ugly’, such as problems of using wholly specific inhibitors of enzymatic H₂S synthesis, and the use of pharmacological donor compounds, which release H₂S too quickly to be physiologically representative of endogenous H₂S synthesis. Furthermore, recently developed slow-release H₂S donors, which offer a more physiological approach to understanding the complex role of H₂S in acute and chronic inflammation (‘the promising’) are discussed.

Keywords::

• β-cyanoalanine
• aminooxyacetate
• arthritis
• asthma
• chronic obstructive pulmonary disorder
• colitis
• cystathionine β-synthase
• cystathionine γ-lyase
• GYY4137
• NSAID
• pain
• pancreatitis
• propargylglycine
• shock

Financial & competing interests disclosure

The authors would like to thank the Wellcome Trust (#091725), the European Union FP7 (RedCat #215009) and the Devon Arthritis Appeal Research Trust for continued financial support. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.