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Instituto de Seguridad y Servicios Sociales de los Trabajadores del Estado

2015, Number 2

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Rev Esp Med Quir 2015; 20 (2)

Neuroinflammation and neurotrophic actions of chemokines during a cerebral ischemic process

Blanco-Álvarez VM, Soto-Rodríguez G, González-Barrios JA, Beltrán-Galindo O, Martínez-Fong D, León-Chávez BA

Language: Spanish
References: 36
Page: 184-192
PDF size: 660.00 Kb.


ABSTRACT

The brain is highly vulnerable to hypoxia and ischemia, damage mechanisms have been studied, but the neuroimmunology response was shown to have a dual function, which can cause inflammation and neurogenesis. The inflammatory process involves the participation of glia and microglia as the principal effectors of immunity within the central nervous system, mediating migration, infiltration and accumulation of leukocytes such as macrophages, neutrophils and lymphocytes to brain parenchyma during ischemia. Cerebrovascular disease has been shown that increases the expression of cytokines (IL-1β, TNFα, IFNγ) and chemokines such as CCL2 (MCP-1), CCL5 (RANTES) and CXCL1 (GRO-α) preceding the leukocyte infiltration into the ischemic lesion, acting through its receptor CCR2, CCR5 and CXCR2, respectively. The inflammation contributes to tissue damage during the early phase of the hypoxic-ischemic response and healing during the late phase of cerebral ischemia. In therapeutic strategies has been sought to use new drugs that can block the neuroimmunologic response particularly transcription of chemokines and therefore activation of glia and microglial cells, which could be important for the recovery of patients with ischemic stroke and restore functionality of the brain tissue. However, the neurogenesis can be affected. We have focused this review on the neuroinflammatory, neurotrophic, neurogenic action, including action on proliferation, migration and differentiation of neural progenitor cells by chemokines CCL2, CCL5 and CXCL1 induced neuroinflammatory response during the process of cerebral ischemia.


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