Innate Immunity and Inflammation Post-Stroke: An α7-Nicotinic Agonist Perspective

International Journal of Molecular Sciences

Silke Neumann³  Nicholas J. Shields³  Thomas Balle²  Mary Chebib²  Andrew N. Clarkson¹  Chris Sobey⁴ 

[1] Department of Anatomy, Brain Health Research Centre and Brain Research New Zealand, University of Otago, P.O. Box 913, Dunedin 9054, New ZealandFaculty of Pharmacy, The University of Sydney, Sydney, NSW 2006, Australia;Department of Pathology, University of Otago, Dunedin 9054, New Zealand;;Department of Pathology, University of Otago, Dunedin 9054, New Zealand

关键词: stroke;    inflammation;    nicotinic;    nicotinic acetylcholine receptor agonist;    immune response;    myeloid cells;   

DOI  :  10.3390/ijms161226141

来源: mdpi

【 摘 要 】

Stroke is one of the leading causes of death and long-term disability, with limited treatment options available. Inflammation contributes to damage tissue in the central nervous system across a broad range of neuropathologies, including Alzheimer’s disease, pain, Schizophrenia, and stroke. While the immune system plays an important role in contributing to brain damage produced by ischemia, the damaged brain, in turn, can exert a powerful immune-suppressive effect that promotes infections and threatens the survival of stroke patients. Recently the cholinergic anti-inflammatory pathway, in particular its modulation using α7-nicotinic acetylcholine receptor (α7-nAChR) ligands, has shown potential as a strategy to dampen the inflammatory response and facilitate functional recovery in stroke patients. Here we discuss the current literature on stroke-induced inflammation and the effects of α7-nAChR modulators on innate immune cells.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.