Zasada działania innowacyjnych opakowań aktywnych w przemyśle żywnościowym. Artykuł przeglądowy

Abstract

Heme-Oxygenase-1 (HO-1) is an enzyme responsible for the degradation of heme that can suppress inflammation, through the production of carbon monoxide (CO). It has been shown in several experimental models that genetic and pharmacological induction of HO-1, as well as non-toxic administration of CO can reduce inflammatory diseases, such as endotoxic shock, type-1 diabetes and graft rejection. Recently, it was shown that the HO-1/CO system can alter the function of antigen presenting cells (APCs) and reduce T cell priming, which can be beneficial during immune-driven inflammatory diseases. The molecular mechanisms by which the HO-1 and CO reduce both APCs- and T cell-driven immunity are just beginning to be elucidated. In this article we discuss recent findings related to the immune regulatory capacity of HO-1 and CO at the level of recognition of pathogen-associated molecular patterns (PAMPs) and T cell priming by APCs. Finally, we propose a possible regulatory role for HO-1 and CO over the recently described mitochondria-dependent immunity. These concepts could contribute to the design of new therapeutic tools for inflammation-based diseases. This article is protected by copyright. All rights reserved.