Abstract
Cytokines and chemokines are proteins that coordinate the immune response throughout the body. The dysregulation of cytokines and chemokines is a central feature in the development of neuroinflammation, neurodegeneration, and demyelination both in the central and peripheral nervous systems and in conditions of neuropathic pain. Pathological states within the nervous system can lead to activation of microglia. The latter may mediate neuronal and glial cell injury and death through production of proinflammatory factors such as cytokines and chemokines. These then help to mobilize the adaptive immune response. Although inflammation may induce beneficial effects such as pathogen clearance and phagocytosis of apoptotic cells, uncontrolled inflammation can result in detrimental outcomes via the production of neurotoxic factors that exacerbate neurodegenerative pathology. In states of prolonged inflammation, continual activation and recruitment of effector cells can establish a feedback loop that perpetuates inflammation and ultimately results in neuronal injury. A critical balance between repair and proinflammatory factors determines the outcome of a neurodegenerative process. This review will focus on how cytokines and chemokines affect neuroinflammation and disease pathogenesis in bacterial meningitis and brain abscesses, Lyme neuroborreliosis, human immunodeficiency virus encephalitis, and neuropathic pain.
Highlights
Cytokines are a class of small proteins that act as signaling molecules at picomolar or nanomolar concentrations to regulate inflammation and modulate cellular activities such as growth, survival, and differentiation [1]
This study suggests that minocycline may afford additional therapeutic benefits extending beyond its antimicrobial activity for the treatment of central nervous system (CNS) infectious diseases typified by a pathogenic inflammatory component through its ability to balance beneficial versus detrimental inflammation
The chemokine IL-8, seen to be elevated in the cerebrospinal fluid (CSF) of Lyme neuroborreliosis (LNB) patients [132, 179] and in rhesus microglia, astrocytes, and endothelial cells exposed to Borrelia burgdorferi (Bb) [151,152,153,154], is associated with blood brain barrier (BBB) dysfunction and plays a central role in recruitment of neutrophils and T cells into the CNS during bacterial meningitis [181,182,183]
Summary
Cytokines are a class of small proteins that act as signaling molecules at picomolar or nanomolar concentrations to regulate inflammation and modulate cellular activities such as growth, survival, and differentiation [1]. Chemokines are implicated in many diseases of the nervous system Their primary role is to induce inflammation through the recruitment of leukocytes by their chemotactic activity, they may have direct effects on neuronal cells. Immune activation in the nervous system is associated with pathological conditions such as bacterial and viral infections, autoimmune diseases, and inflammatory neurodegenerative disorders including AD, PD, amyotrophic lateral sclerosis, MS [41,42,43,44], and Lyme neuroborreliosis (LNB) [45] Peripheral neuropathies such as Guillain-Barresyndrome [46], PNS Lyme neuroborreliosis [47], demyelinating polyradiculoneuropathies [48], and conditions of neuropathic pain [10, 49] are accompanied by inflammation. This review will focus on how cytokines and chemokines affect neuroinflammation and disease pathogenesis in bacterial meningitis and brain abscesses, Lyme neuroborreliosis, human immunodeficiency virus encephalitis (HIVE), and neuropathic pain
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