Formyl peptide receptors: A promiscuous subfamily of G protein-coupled receptors controlling immune responses

Migeotte, Isabelle; Communi, David; Parmentier, Marc

doi:10.1016/j.cytogfr.2006.09.009

Cited by 373 publications

(405 citation statements)

References 148 publications

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“…Interestingly, lipoxin A 4 , which is thought to be an endogenous lipid ligand for FPR2/ALX, exerts anti-inflammatory and pro-resolving effects including the inhibition of neutrophil migration. 1,[4][5][6] In mice, eight formyl peptide receptor genes have been identified, 3,7 and mouse Fpr1 and Fpr2 are considered to be the receptors homologous to human FPR1 and FPR2/ALX, respectively. 3,8 Mouse neutrophils also express both Fpr1 and Fpr2.…”

Section: Discussionmentioning

confidence: 99%

“…1,[4][5][6] In mice, eight formyl peptide receptor genes have been identified, 3,7 and mouse Fpr1 and Fpr2 are considered to be the receptors homologous to human FPR1 and FPR2/ALX, respectively. 3,8 Mouse neutrophils also express both Fpr1 and Fpr2. 8 The biological functions of these receptors in neutrophil migration in vivo, however, are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

“…FPR2/ALX was identified as a low-affinity receptor for fMLF, but accumulating evidence has revealed that the receptor interacts with a wide variety of structurally unrelated ligands. 3 The biological effects of these ligands on neutrophil chemotaxis vary depending on the ligand. Interestingly, lipoxin A 4 , which is thought to be an endogenous lipid ligand for FPR2/ALX, exerts anti-inflammatory and pro-resolving effects including the inhibition of neutrophil migration.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of neutrophil migration in mice by mouse formyl peptide receptors 1 and 2 dual agonist: indication of cross-desensitization in vivo

et al. 2010

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Summary It has been reported that the stimulation of neutrophils with N‐formyl‐Met‐Leu‐Phe (fMLF), an agonist for formyl peptide receptor (Fpr) 1, renders cells unresponsive to other chemoattractants in vitro. This is known as cross‐desensitization, but its functional relevance in neutrophil migration in vivo has not been investigated. Here, we show that precedent stimulation of mouse neutrophils with compound 43, a non‐peptidyl agonist for mouse Fpr1 and Fpr2, rendered the cells unresponsive to a second stimulation with C5a, leukotriene B4, or keratinocyte‐derived cytokine (KC) in calcium mobilization and chemotaxis assays in vitro. The expression of chemokine (C‐X‐C motif) receptor 2 (CXCR2) on the surface of neutrophils was concomitantly diminished by stimulating the cells with the compound. Moreover, oral administration of the compound to mice before they were exposed to lipopolysaccharide (LPS) aerosol resulted in a dose‐dependent reduction in the neutrophil count in bronchoalveolar lavage fluid. The expression of CXCR2 on blood neutrophils was also reduced in the compound‐administered mice. The recipient mice that underwent adoptive transfer of fluorescence‐labelled neutrophils that had been incubated with the compound showed a substantial decrease in neutrophil counts in bronchoalveolar lavage fluid after they were exposed to LPS, when compared with the control mice to which vehicle‐treated neutrophils had been transferred. These results are consistent with the idea that the agonist for Fpr1 and Fpr2 induced cross‐desensitization in neutrophils and attenuated neutrophil migration into the airways. Our results also revealed the unpredicted effect of an Fpr1 and Fpr2 dual agonist, which may act as a functional antagonist for multiple chemoattractant receptors in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Inhibition of neutrophil migration in mice by mouse formyl peptide receptors 1 and 2 dual agonist: indication of cross-desensitization in vivo

et al. 2010

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“…There are three structurally-related FPRs in humans, known as FPR1, FPR2 and FPR3 [31]. Functionally, FPRs sense and bind to peptides that harbor a bacterial specific Nformyl group of which an example is N-formyl methionyl-leucyl-phenylalanine (fMLF).…”

Section: Epithelial Perception and Monitoring Of The Microbiotamentioning

confidence: 99%

Redox signaling mediated by the gut microbiota

Jones

Neish

2017

Free Radical Biology and Medicine

141

101

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“…FPR2 is expressed by various kinds of inflammatory cells, including macrophages, monocytes, neutrophils, T lymphocytes, bronchial epithelial cells and microvascular endothelial cells. 16,17 These inflammatory cells are involved in the pathogenesis of asthma and in asthmatic subphenotypes, including aspirin hypersensitivity. On the basis of these biological functions, genetic alterations in FPR2 may be postulated to contribute to the pathophysiological processes of AERD.…”

Section: Introductionmentioning

confidence: 99%

Association analysis of formyl peptide receptor 2 (FPR2) polymorphisms and Aspirin exacerbated respiratory diseases

et al. 2012

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Aspirin-exacerbated respiratory diseases (AERD) are associated with the metabolism of arachidonic acid. FPR2 (formyl peptide receptor2) is a high-affinity ligand receptor for potent anti-inflammatory lipid metabolites: lipoxins. Thus, functional alterations of the FPR2 may contribute to AERD. We investigated the relationship between single-nucleotide polymorphisms (SNPs) in the FPR2 and AERD. Asthmatics were categorized into AERD o15% decreases in forced expiratory volume in one second (FEV 1 ), and/or naso-ocular reactions after oral aspirin challenge (n¼170) and aspirin-tolerant asthma (ATA, n¼268). In all, 11 SNPs were genotyped. FPR2 protein expressions on CD14-positive monocytes in peripheral blood were measured using flow cytometric analysis. We performed RT-PCR of the FPR2 mRNA expressed by peripheral blood mononuclear cells. Logistic regression analysis showed that the minor allele frequency of FPR2 À4209T4G (rs1769490) in intron 2 was significantly lower in the AERD group (n¼170) than in the ATA group (n¼268) (P¼0.006, P corr ¼0.04, recessive model). The decline of FEV 1 after aspirin challenge was significantly lower in the subjects with GG homozygotes of FPR2 À4209T4G than those with the other genotypes (P¼0.0002). Asthmatic homozygotes for FPR2 À4209T4G minor allele exhibited significantly higher FPR2 protein expression in CD14-positive monocytes than did those with the common allele of FPR2 À4209T4G allele (P¼0.01). There was no difference in the expression of the wild form and the exon 2 deleted variant form of FPR2 gene according to the genotypes of FPR2 À4209T4G. The minor allele at FPR2 À4209T4G may have a protective role against the development of AERD, via increase of FPR2 protein expression in inflammatory cells.

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Formyl peptide receptors: A promiscuous subfamily of G protein-coupled receptors controlling immune responses

Cited by 373 publications

References 148 publications

Inhibition of neutrophil migration in mice by mouse formyl peptide receptors 1 and 2 dual agonist: indication of cross-desensitization in vivo

Inhibition of neutrophil migration in mice by mouse formyl peptide receptors 1 and 2 dual agonist: indication of cross-desensitization in vivo

Redox signaling mediated by the gut microbiota

Association analysis of formyl peptide receptor 2 (FPR2) polymorphisms and Aspirin exacerbated respiratory diseases

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