The dual role of the neuroinflammatory response after ischemic stroke: modulatory effects of hypothermia
- PDF / 781,492 Bytes
- 18 Pages / 595.276 x 793.701 pts Page_size
- 99 Downloads / 198 Views
REVIEW
JOURNAL OF NEUROINFLAMMATION
Open Access
The dual role of the neuroinflammatory response after ischemic stroke: modulatory effects of hypothermia An-Gaëlle Ceulemans1, Tine Zgavc1, Ron Kooijman2, Said Hachimi-Idrissi3, Sophie Sarre1*, Yvette Michotte1
Abstract Neuroinflammation is a key element in the ischemic cascade after cerebral ischemia that results in cell damage and death in the subacute phase. However, anti-inflammatory drugs do not improve outcome in clinical settings suggesting that the neuroinflammatory response after an ischemic stroke is not entirely detrimental. This review describes the different key players in neuroinflammation and their possible detrimental and protective effects in stroke. Because of its inhibitory influence on several pathways of the ischemic cascade, hypothermia has been introduced as a promising neuroprotective strategy. This review also discusses the influence of hypothermia on the neuroinflammatory response. We conclude that hypothermia exerts both stimulating and inhibiting effects on different aspects of neuroinflammation and hypothesize that these effects are key to neuroprotection. Introduction Inflammation is an essential tool to defend oneself against infectious organisms. However, it becomes detrimental when it is prolonged or attacks self antigens [1]. Stroke and neurodegenerative diseases such as Alzheimer’s disease, multiple sclerosis and Parkinson’s disease are associated with a chronic inflammatory response [2,3]. After ischemic stroke, the death of ischemic neurons and especially the release of necrotic cell debris triggers inflammation resulting in strong activation of phagocytic cells [1,4]. Over the past two decades, our understanding of the inflammatory response after stroke and in other diseases has increased due to extensive research. Previously, it was thought that the inflammatory response in brain was beneficial and necessary for repair. Later, it became clear that this “neuro” inflammatory response could be detrimental too, and that even peripheral immune responses can be regulated by the brain [5]. Furthermore, injury to the brain can make the body more vulnerable to systemic infections. For example, a central nervous system injury-induced immunodepression syndrome has been identified in experimental * Correspondence: [email protected] 1 Department of Pharmaceutical Chemistry and Drug Analysis, Research Group Experimental Neuropharmacology, Vrije Universiteit Brussel, Laarbeeklaan 103, 1090 Brussels, Belgium Full list of author information is available at the end of the article
stroke models leading to spontaneous systemic bacterial infections within 3 days after stroke [6-8].
Stroke Stroke is a broad term that includes conditions caused by occlusion of or hemorrhage from a blood vessel supplying the brain [7,9]. Its incidence remains high and the number of approved therapies low. As our society ages, the number of stroke patients continues to increase, and will become an important socio-economic burden, as 80% of patients who survive
Data Loading...
