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Reactive astrocytosis seems to be strongly implicated in the development and maintenance of inflammatory and neurodegenerative disorders.
The present study suggests that 5-HT2A receptors were involved in the maintenance of inflammatory pain, and that 5-HT suppressed inflammation-associated endogenous opioid analgesia contributing to its pro-nociceptive actions in the periphery.
In this review, we will explore the different animal models of RA, and their contribution to elucidating the role that effector T cells play in the regulation, induction, and maintenance of inflammatory joint disease.
Preclinical animal models suggest that the CCL2-CCR2 axis has a critical role in the development and maintenance of inflammatory disease states (e.g., multiple sclerosis, atherosclerosis, insulin resistance, restenosis, and neuropathic pain), which can be treated through inhibition of the CCR2 receptor.
In particular, mitogen-activated protein kinase (MAPK), such as ERK and p38, is activated by inflammatory mediators in primary sensory and secondary order dorsal horn neurons and participates in the generation and maintenance of inflammatory pain.
A CSD-induced neuronal megachannel opening may therefore promote sustained stimulus required for both sensitization and activation of meningeal trigeminal afferents through the maintenance of inflammatory responses which may be involved in the subsequent headache pain.
Similar(36)
The inadequate clearance of these viral agents and/or the consequent damage of the epithelial cells initiate a cascade of events that may lead to the self-maintenance of inflammatory mechanisms and induction of autoimmune manifestations.
Sulphasalazine, metronidazole and more recently, modified forms of 5-aminosalicylic acid are used for maintenance therapy of inflammatory bowel disease.
It is known that local inflammation is related to wound healing; however, the maintenance of the inflammatory reaction can impair the proliferation and migration of oral mucosal cells.
The review will also highlight the important interplay between neurons and non-neuronal cells (i.e., microglia and astrocytes) within the dorsal horn of the spinal cord in the generation and maintenance of chronic inflammatory and neuropathic pain.
Here, we tested the hypothesis that intrathecally applied ketamine or morphine not only reduce pain-related behavior, but also attenuate induction and maintenance of the inflammatory response in a model of chronic antigen-induced arthritis (AIA).
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