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Curr Neuropharmacol. 2019 Oct 19. doi: 10.2174/1570159X17666191019170244. [Epub ahead of print]

The contribution of formyl peptide receptor dysfunction to the course of neuroinflammation: A potential role in the brain pathology.

Author information

1
Laboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smętna St. 31-343 Kraków. Poland.
2
Department of Pharmacy - Drug Sciences, University of Bari, via Orabona 4, 70125 Bari. Italy.

Abstract

Chronic inflammatory processes within the central nervous system (CNS) are in part responsible for the development of neurodegenerative and psychiatric diseases. These processes are associated with, among other things, the increased and disturbed activation of microglia and the elevated production of proinflammatory factors. Recent studies have indicated that the disruption of the process of resolution of inflammation (RoI) may be the cause of CNS disorders. It has been shown that the RoI is regulated by endogenous molecules called specialized pro-resolving mediators (SPMs), which interact with specific membrane receptors. Some SPMs activate formyl peptide receptors (FPRs), which belong to the family of seven-transmembrane G protein-coupled receptors. These receptors take part not only in the proinflammatory response but also in the resolution of inflammation process. Therefore, the activation of FPRs might have complex consequences. This review discusses the potential role of FPRs, and in particular the role of FPR2 subtype, in the brain under physiological and pathological conditions and their involvement in processes underlying neurodegenerative and psychiatric disorders as well as ischemia, the pathogenesis of which involves the dysfunction of inflammatory processes.

KEYWORDS:

Alzheimer's disease; depression; formyl peptide receptors; glial cells; ischemia; neuroinflammation; new pro-resolving agonists; resolution of inflammation

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