ArticleInflammation2007
Cyclosporin H, Boc-MLF and Boc-FLFLF are antagonists that preferentially inhibit activity triggered through the formyl peptide receptor.
Article in Inflammation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
63 citing papers in PubMed, 137 citations in OpenAlex.
- N-Formyl Methionine Peptide-Mediated Neutrophil Activation in Systemic Sclerosis.Frontiers in immunology · 2021Trial
- Genome-wide CRISPR screening identifies Annexin A1 as a facilitator of porcine astrovirus entry.PLoS pathogens · 2026Article
- Human neutrophils recognize group B streptococciFrontiers in immunology · 2026Article
- Involvement of formyl peptide receptor 2 in canine coronavirus infection: in vitro and in Silico approaches.Virology journal · 2025Article
- Article
- The Role of Endogenous Specialized Proresolving Mediators in Mast Cells and Their Involvement in Inflammation and Resolution.International journal of molecular sciences · 2025Review
- Differential requirement of formyl peptide receptor 1 in macrophages and neutrophils in the host defense against Mycobacterium tuberculosis Infection.Scientific reports · 2024Article
- Differential requirement of Formyl Peptide Receptor 1 in macrophages and neutrophils in the host defense againstResearch square · 2024Article
- An overview of the regulatory role of annexin A1 in the tumor microenvironment and its prospective clinical application (Review).International journal of oncology · 2024Review
- Article
- Development of ADS051, an oral, gut-restricted, small molecule neutrophil modulator for the treatment of neutrophil-mediated inflammatory diseases.FEBS open bio · 2023Article
- BacSp222 bacteriocin as a novel ligand for TLR2/TLR6 heterodimer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Properties and fate of human mesenchymal stem cells upon miRNA let-7f-promoted recruitment to atherosclerotic plaques.Cardiovascular research · 2023Article
- ModifiedFrontiers in molecular biosciences · 2023Article
- Suppression of annexin A1 and its receptor reduces herpes simplex virus 1 lethality in mice.PLoS pathogens · 2022Article
- Neutrophils discriminate live from dead bacteria by integrating signals initiated by Fprs and TLRs.The EMBO journal · 2022Article
- Effects of Formyl Peptide Receptor Agonists AcCells · 2022Article
- Exosomes mediate LTB4 release during neutrophil chemotaxis.PLoS biology · 2021Article
- Functional selective FPR1 signaling in favor of an activation of the neutrophil superoxide generating NOX2 complex.Journal of leukocyte biology · 2021Article
- Resolvin D1 Attenuates Innate Immune Reactions in Experimental Subarachnoid Hemorrhage Rat Model.Molecular neurobiology · 2021Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to properly interpret receptor inhibition experiments, the precise receptor specificities of the employed antagonists are of crucial importance. Lately, a great number of agonists for various formyl peptide receptors have been identified using a selection of antagonists. However, some confusion exists as to the precise receptor specificities of many of these antagonists. We have investigated the effects of formyl peptide receptor family antagonists on the neutrophil response induced by agonists for the formyl peptide receptor (FPR) and the formyl peptide receptor like 1 (FPRL1). To determine FPR- and FPRL1-specific interactions, these antagonists should not be used at used at concentrations above 10 microM. Signaling through FPR was inhibited by low concentrations of the antagonists cyclosporin H, Boc-MLF (also termed Boc-1), and Boc-FLFLFL (also termed Boc-2), while higher concentrations also partly inhibited the signaling through FPRL1. The antagonist WRWWWW (WRW(4)) specifically inhibited the signaling through FPRL1 at low concentrations but at high concentrations also partly the signaling through FPR. Based on the difference in potency of cyclosporin H and the two Boc-peptides, we suggest using cyclosporin H as a specific inhibitor for FPR. To specifically inhibit the FPRL1 response the antagonist WRW(4) should be used.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.