Heme oxygenase-1 and carbon monoxide: emerging therapeutic targets in inflammation and allergy

Recent Pat Inflamm Allergy Drug Discov. 2008 Nov;2(3):159-65. doi: 10.2174/187221308786241929.

Abstract

Cumulative evidence suggests that the induction of the antioxidant/anti-inflammatory heme oxygenase (HO)-1 may play a protective role in allergic inflammation. HO-1 suppresses mast cell degranulation and cytokine synthesis. The up-regulation of the HO-1 pathway has a significant protective effect against airway inflammation, mucus hyper-secretion, and hyper-responsiveness in a model of allergic asthma. Moreover, HO-1 inhibits T cell-dependent skin inflammation and differentiation and function of antigen-presenting cells. The precise underlying mechanisms for HO-1-based protection against allergic inflammation are not yet completely understood, but appear to involve the protective effects of HO-1 by-products, such as carbon monoxide (CO), biliverdin/bilirubin and free iron. Among the HO-1 by-products, CO has been shown to mimic some protective actions of HO-1 in allergic inflammations. This article reviews the latest knowledge, recent patent and studies on the protective roles and mechanisms of HO-1/CO in inflammation and allergy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Carbon Monoxide / metabolism*
  • Drug Delivery Systems*
  • Heme Oxygenase-1 / metabolism*
  • Humans
  • Hypersensitivity / drug therapy
  • Hypersensitivity / physiopathology
  • Inflammation / drug therapy
  • Inflammation / physiopathology
  • Patents as Topic
  • Up-Regulation

Substances

  • Carbon Monoxide
  • Heme Oxygenase-1