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Contribution of Receptors, Transcription Factors, and Genes in the Induction of Neuroinflammation

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Inflammation and Oxidative Stress in Neurological Disorders

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Abstract

Neuroinflammation, a neuroprotective process, which facilitates recovery is “driven” by activated resident glial cells (astrocytes and microglia). The activation of glial cells is accompanied by increase in production of TNF-α, IL-1β, and IL-6, chemokines, NO, prostaglandin E2, PAF, and ROS along with invasion of circulating immune cells, which secrete more proinflammatory cytokines. Increase in cytokines is promoted by increase in inflammatory signaling pathways, which involve the participation of Jun N-terminal kinase (JNK), IκB kinase (IKK)-β, nuclear factor (NF)-κB, and redox-sensitive transcription factor. Microglial activation may not only increase oxidative stress through the generation of proinflammatory cytokines, but also through the production of nitric oxide. Proinflammatory cytokines and high nityric oxide levels may promote ROS formation, which in turn accelerates lipid peroxidation, damaging membrane phospholipids. Collectively, these processes initiate and establish uncontrolled brain damage pathway for the pathogenesis of neurodegenerative diseases.

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    Akhlaq A. Farooqui

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Farooqui, A. (2014). Contribution of Receptors, Transcription Factors, and Genes in the Induction of Neuroinflammation. In: Inflammation and Oxidative Stress in Neurological Disorders. Springer, Cham. https://doi.org/10.1007/978-3-319-04111-7_4

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