Signaling by neutrophil G protein-coupled receptors that regulate the release of superoxide anions.

Autor:	Dahlgren C; Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gulhedsgatan 10, Göteborg S-41346, Sweden., Forsman H; Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gulhedsgatan 10, Göteborg S-41346, Sweden., Sundqvist M; Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gulhedsgatan 10, Göteborg S-41346, Sweden., Björkman L; Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gulhedsgatan 10, Göteborg S-41346, Sweden., Mårtensson J; Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gulhedsgatan 10, Göteborg S-41346, Sweden.
Jazyk:	angličtina
Zdroj:	Journal of leukocyte biology [J Leukoc Biol] 2024 Nov 27; Vol. 116 (6), pp. 1334-1351.
DOI:	10.1093/jleuko/qiae165
Abstrakt:	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. Danger signaling molecular patterns such as the N-formylated peptides that are formed during bacterial and mitochondrial protein synthesis and recognized by formyl peptide receptors (FPRs) and free fatty acids recognized by free fatty acid receptors (FFARs) regulate neutrophil functions. Short peptides and short-chain fatty acids activate FPR1 and FFA2R, respectively, while longer peptides and fatty acids activate FPR2 and GPR84, respectively. The activation profiles of these receptors include the release of reactive oxygen species (ROS) generated by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Activation of the oxidase and the production of ROS are processes that are regulated by proinflammatory mediators, including tumor necrosis factor α and granulocyte/macrophage colony-stimulating factor. The receptors have signaling and functional similarities, although there are also important differences, not only between the two closely related neutrophil FPRs, but also between the FPRs and the FFARs. In neutrophils, these receptors never walk alone, and additional mechanistic insights into the regulation of the GPCRs and the novel regulatory mechanisms underlying the activation of NADPH oxidase advance our understanding of the role of receptor transactivation in the regulation of inflammatory reactions. Competing Interests: Conflict of interest statement. The authors declare no conflict of interest. (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Leukocyte Biology.)
Databáze:	MEDLINE
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