[No Title Available]

Abstract

Hemolytic episodes such as sickle cell disease, malaria and ischemia-reperfusion occurrence are often associated to the statement of an inflammatory response which may develop or not to a chronic inflammatory status. Although these pathological states are triggered by distinct etiological agents, all of them are associated to high levels of free heme in circulation. In this review, we aim to focus the very recent achievements that have led to the statement of free heme as a proinflammatory molecule, which may play a central role during the onset and/or persistance of inflammation during these pathologies.

Protection against Heme Toxicity: Hemopexin Rules, OK?

“…The effects of heme on cells that act in innate immunity has been reviewed. 157 Even in the absence of a stimulator such as LPS, heme triggers the NADPH-dependent oxidative burst of neutrophils 158 and induces neutrophil migration in vivo and in vitro, 159 in part due to the induction of HO1 activity. The ROS production occurs via the activation of a G-protein coupled receptor (GPR) with some partial contribution from the phosphoinositide-3 kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways.…”