Heme oxygenase-1 and carbon monoxide regulate intestinal homeostasis and mucosal immune responses to the enteric microbiota

Abstract

Heme oxygenase-1 (HO-1) and its enzymatic by-product carbon monoxide (CO) have emerged as important regulators of acute and chronic inflammation. Mechanisms underlying their anti-inflammatory effects are only partially understood. In this addendum, we summarize current understanding of the role of the HO-1/CO pathway in regulation of intestinal inflammation with a focus on innate immune function. In particular, we highlight our recent findings that HO-1 and CO ameliorate intestinal inflammation through promotion of bacterial clearance. Our work and that of many others support further investigation of this global homeostatic pathway in the human inflammatory bowel diseases (IBDs).

Keywords: :

• Crohn disease
• ulcerative colitis
• macrophage
• heme oxygenase
• carbon monoxide

This article refers to:

10.4161/gmic.27290

Disclosure of Potential Conflicts of Interest

No potential conflict of interest was disclosed.

Acknowledgments

We thank all contributors to the original article. This work was supported in part by National Institutes of Health grants R01 DK54452, Gastroenterology Research Training grant T32 DK007737, National Research Service Award F32 DK083186, and a Crohn’s and Colitis Foundation of America Research Fellowship Award.