Abstract
The concept of central nervous system (CNS) inflammation has evolved over the last decades. Neuroinflammation is the response of reactive CNS components to altered homeostasis, regardless of the cause to be endogenous or exogenous. Neurological diseases, whether traumatic, neoplastic, ischemic, metabolic, toxic, infectious, autoimmune, developmental, or degenerative, involve direct and indirect immune-related neuroinflammation. Brain infiltrates of the innate and adaptive immune system cells appear in response to an infective or otherwise noxious agent and produce inflammatory mediators. Mediators of inflammation include local and recruited cells and signals. Processes derived from extrinsic and intrinsic CNS diseases also elicit the CNS inflammatory response. A deeper understanding of immune-related inflammation in health and disease is necessary to find potential therapeutic targets for preventing or reducing CNS damage. This review is aimed at discussing the innate and adaptive immune system functions and their roles in regulating brain cell responses in disease and homeostasis maintenance.
Highlights
The cardinal signs of acute inflammatory diseases involve cellular and molecular events, typically self-limiting, unlike autoimmune and neurodegenerative lesions, which are due to the failure in chronic inflammation resolution
This review offers an update on the key inflammatory mediators and the role of inflammatory cells in infectious and noninfectious conditions on neuroinflammation
This accounts for a regulation of Mitochondrial antiviral signaling (MAVS)-dependent microglial activation in the central nervous (CNS), where autophagy has a key role in microglia-driven inflammatory brain diseases
Summary
The cardinal signs of acute inflammatory diseases involve cellular and molecular events, typically self-limiting, unlike autoimmune and neurodegenerative lesions, which are due to the failure in chronic inflammation resolution. This implies sustained recruitment and persistence of inflammatory cells at the site of inflammation because of lacking apoptosis and dead cell clearance, macrophages not switching to an anti-inflammatory/regenerative phenotype, no way out for the effector cells, and partial tissue regeneration Some of these unsuccessful resolution phase scenarios appear common to acute and chronic diseases. The nervous system lays out functional connections with the immune system directly innervating the lymphoid system with adrenergic, peptidergic, and catecholaminergic fibers and via receptors for neuropeptides (substance P (SP), somatostatin, and vasointestinal peptide, (VIP)) and neurotransmitters (noradrenaline, acetylcholine, enkephalin, and endorphin) on immune cells These mediators can modulate the synthesis and release of cytokines, including the chemokines, chemotactic cytokines. We discuss the relationship between neuroinflammatory processes, hypoxia, and oxidative stress and how innate and adaptive immunity shape up an integrative network to regulate immunological processes, affecting brain homeostasis
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