Human neutrophils are components of the innate immune system and are the most abundant white blood cells in the circulation. They are professional phagocytes and express several G protein-coupled receptors (GPCRs), which are essential for proper neutrophil functions. So far, the two formyl peptide receptors, FPR1 and FPR2, have been the most extensively studied group of neutrophil GPCRs, but recently, a new group, the free fatty acid (FFA) receptors, has attracted growing attention. Neutrophils express two FFA receptors, GPR84 and FFA2, which sense medium- and short-chain fatty acids respectively, and display similar activation profiles. The exact pathophysiological role of GPR84 is not yet fully understood, but it is generally regarded as a pro-inflammatory receptor that mediates neutrophil activation. In this review, we summarize current knowledge of how GPR84 affects human neutrophil functions and discuss the regulatory mechanisms that control these responses, focusing on the similarities and differences in comparison to the two FPRs and FFA2. LINKED ARTICLES: This article is part of a themed issue GPR84 Pharmacology. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.10/issuetoc.
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http://dx.doi.org/10.1111/bph.16066 | DOI Listing |
Cancers (Basel)
December 2024
Laboratory of Pharmacology, Department of Medicine, Democritus University of Thrace, 68100 Alexandroupolis, Greece.
Hum Immunol
November 2024
Department of Pathology, Anyang Tumor Hospital, The Affiliated Anyang Tumor Hospital of Henan University of Science and Technology, Anyang 455000, China. Electronic address:
Background: It is reported that G protein-coupled receptor 84 (GPR84) can participate in inflammation and immune regulation to repress anti-tumor responses. However, the function of GPR84 in lung cancer (LC) and its potential molecular mechanisms are still largely unknown.
Methods: Bioinformatics and molecular experiments were employed to assess the expression of GPR84 in LC.
Acta Neuropathol Commun
September 2024
INSERM UMR 968, CNRS UMR 7210, Institut de la Vision, IHU FOReSIGHT, Sorbonne Université UM80, 75012, Paris, France.
Background: Glaucoma is a leading cause of blindness, affecting retinal ganglion cells (RGCs) and their axons. By 2040, it is likely to affect 110 million people. Neuroinflammation, specifically through the release of proinflammatory cytokines by M1 microglial cells, plays a crucial role in glaucoma progression.
View Article and Find Full Text PDFCell Chem Biol
August 2024
Department of Chemistry, Yale University, New Haven, CT 06520, USA; Institute of Biomolecular Design & Discovery, Yale University, West Haven, CT 06516, USA; Department of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT 06536, USA. Electronic address:
Altered human aldo-keto reductase family 1 member C3 (AKR1C3) expression has been associated with poor prognosis in diverse cancers, ferroptosis resistance, and metabolic diseases. Despite its clinical significance, the endogenous biochemical roles of AKR1C3 remain incompletely defined. Using untargeted metabolomics, we identified a major transformation mediated by AKR1C3, in which a spermine oxidation product "sperminal" is reduced to "sperminol.
View Article and Find Full Text PDFJ Leukoc Biol
November 2024
Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gulhedsgatan 10, Göteborg S-41346, Sweden.
In human peripheral blood, the neutrophil granulocytes (neutrophils) are the most abundant white blood cells. These professional phagocytes are rapidly recruited from the bloodstream to inflamed tissues by chemotactic factors that signal danger. Neutrophils, which express many receptors that are members of the large family of G protein-coupled receptors (GPCRs), are critical for the elimination of pathogens and inflammatory insults, as well as for the resolution of inflammation leading to tissue repair.
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