Abstract
Ischemic stroke is the most frequent cause of persistent neurologic disability in modern Western societies. Albeit it is still not clear whether inflammation is merely an epiphenomenon or rather has a disease-promoting function, accumulating evidence implicates inflammation in many forms of acute neurodegenerative disorders including ischemia. The immune cell influx during a neuropathological event is thought to be elicited by glial cells, especially microglia. This article reviews the cellular and molecular pathways involved in stroke-induced inflammatory response in the CNS. We focused on how CNS innate immune cells including microglia and macrophages play integral roles in receiving and propagating inflammatory signals, and how activated microglia secrete a wide range of factors. We present the relevance of the expression of adhesion molecules after ischemia including selectin, immunoglobulin superfamily, integrins, and the role of inflammatory mediators such as cytokines, chemokines and matrix metalloproteinases. Further, we explore the role of transcription factors in inflammation, and the function of immunomodulation and innate and adaptive immunity in brain ischemia, focusing on immunosupression therapies for acute stroke. Although several approaches for anti-inflammatory treatment have proven effective in animal models, clinical trials of immune system modulation therapy after stroke have not yet proved successful. There is still much to be done in order to translate interesting findings into therapies, but undoubtedly studying the cellular and molecular pathways may not only improve our understanding of inflammatory mechanism but also serve as a basis for designing effective therapies.
Keywords: Ischemic stroke, inflammation, glial cells, molecular pathways, immune cells, immunoglobulin superfamily, integrins, cytokines
Current Pharmaceutical Design
Title: Inflammation as Therapeutic Objective in Stroke
Volume: 14 Issue: 33
Author(s): Joaquin Jordan, Tomas Segura, David Brea, Maria F. Galindo and Jose Castillo
Affiliation:
Keywords: Ischemic stroke, inflammation, glial cells, molecular pathways, immune cells, immunoglobulin superfamily, integrins, cytokines
Abstract: Ischemic stroke is the most frequent cause of persistent neurologic disability in modern Western societies. Albeit it is still not clear whether inflammation is merely an epiphenomenon or rather has a disease-promoting function, accumulating evidence implicates inflammation in many forms of acute neurodegenerative disorders including ischemia. The immune cell influx during a neuropathological event is thought to be elicited by glial cells, especially microglia. This article reviews the cellular and molecular pathways involved in stroke-induced inflammatory response in the CNS. We focused on how CNS innate immune cells including microglia and macrophages play integral roles in receiving and propagating inflammatory signals, and how activated microglia secrete a wide range of factors. We present the relevance of the expression of adhesion molecules after ischemia including selectin, immunoglobulin superfamily, integrins, and the role of inflammatory mediators such as cytokines, chemokines and matrix metalloproteinases. Further, we explore the role of transcription factors in inflammation, and the function of immunomodulation and innate and adaptive immunity in brain ischemia, focusing on immunosupression therapies for acute stroke. Although several approaches for anti-inflammatory treatment have proven effective in animal models, clinical trials of immune system modulation therapy after stroke have not yet proved successful. There is still much to be done in order to translate interesting findings into therapies, but undoubtedly studying the cellular and molecular pathways may not only improve our understanding of inflammatory mechanism but also serve as a basis for designing effective therapies.
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Cite this article as:
Jordan Joaquin, Segura Tomas, Brea David, Galindo F. Maria and Castillo Jose, Inflammation as Therapeutic Objective in Stroke, Current Pharmaceutical Design 2008; 14 (33) . https://dx.doi.org/10.2174/138161208786848766
DOI https://dx.doi.org/10.2174/138161208786848766 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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