ArticleImmunology2004
The mechanism for activation of the neutrophil NADPH-oxidase by the peptides formyl-Met-Leu-Phe and Trp-Lys-Tyr-Met-Val-Met differs from that for interleukin-8.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 82 citations in OpenAlex.
- The effect of a selective CXCR2 antagonist (AZD5069) on human blood neutrophil count and innate immune functions.British journal of clinical pharmacology · 2015Trial
- The free fatty acid 2 receptor regulates C5a induced neutrophil superoxide production and its sensitivity to inhibition by the antagonist avacopan.Frontiers in immunology · 2026Article
- Neutrophil extracellular traps and cannabinoids: potential in cancer metastasis.Frontiers in oncology · 2025Review
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- Functional selective FPR1 signaling in favor of an activation of the neutrophil superoxide generating NOX2 complex.Journal of leukocyte biology · 2021Article
- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- Interleukin 8 Elicits Rapid Physiological Changes in Neutrophils That Are Altered by Inflammatory Conditions.Journal of innate immunity · 2021Article
- The Two Formyl Peptide Receptors Differently Regulate GPR84-Mediated Neutrophil NADPH Oxidase Activity.Journal of innate immunity · 2021Article
- Innate Immunity and Cell Surface Receptors in the Pathogenesis of COPD: Insights from Mouse Smoking Models.International journal of chronic obstructive pulmonary disease · 2020Review
- A Role for MK2 in Enhancing Neutrophil-Derived ROS Production and Aggravating Liver Ischemia/Reperfusion Injury.Frontiers in immunology · 2018Article
- The Lipidated Peptidomimetic Lau-((S)-Aoc)-(Lys-βNphe)6-NH2 Is a Novel Formyl Peptide Receptor 2 Agonist That Activates Both Human and Mouse Neutrophil NADPH Oxidase.The Journal of biological chemistry · 2016Article
- The subcellular localization of the receptor for platelet-activating factor in neutrophils affects signaling and activation characteristics.Clinical & developmental immunology · 2013Article
- Article
- Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis.Journal of leukocyte biology · 2010Article
- The annexin I sequence gln(9)-ala(10)-trp(11)-phe(12) is a core structure for interaction with the formyl peptide receptor 1.The Journal of biological chemistry · 2010Article
- Evidence that cathelicidin peptide LL-37 may act as a functional ligand for CXCR2 on human neutrophils.European journal of immunology · 2009Article
- International Union of Basic and Clinical Pharmacology. LXXIII. Nomenclature for the formyl peptide receptor (FPR) family.Pharmacological reviews · 2009Review
- Respiratory burst function of ovine neutrophils.BMC immunology · 2009Article
- Formyl-methionyl-leucyl-phenylalanine-induced dopaminergic neurotoxicity via microglial activation: a mediator between peripheral infection and neurodegeneration?Environmental health perspectives · 2008Article
- Neutrophils from p40phox-/- mice exhibit severe defects in NADPH oxidase regulation and oxidant-dependent bacterial killing.The Journal of experimental medicine · 2006Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophil chemotaxis has been shown to be regulated by two different signalling pathways that allow strong chemoattractants, such as bacterial-derived formylated peptides, to dominate over endogenous attractants, such as interleukin-8 (IL-8). Here we show that triggering of the formyl peptide receptor (FPR) with f-Met-Leu-Phe (fMLF) substantially reduced the neutrophil superoxide production induced by activation of the CXC receptors with IL-8. When the order of agonists was reversed, the cells were primed in their response to fMLF, suggesting that the signalling hierarchy between strong, so-called end-type (i.e. fMLF) and weak or intermediate-type (i.e. IL-8) chemoattractants, is also operating during activation of the NADPH-oxidase. The same result was obtained when fMLF was replaced with the hexapeptide, WKYMVM, specific for the formyl peptide-like receptor 1 (FPRL1). There were additional differences between the agonist receptor pairs fMLF/FPR, WKYMVM/FPRL1 and IL-8/CXCR. In contrast to FPR and FPRL1, no reserve pool of CXCR was present in subcellular granules and it was impossible to prime the oxidative response transduced through CXCR by the addition of priming agents such as tumour necrosis factor-alpha and platelet-activating factor. Moreover, the cytoskeleton-disrupting substance, cytochalasin B, had no effect either on IL-8-triggered oxidase activation or on CXCR reactivation. A pertussis toxin-sensitive G-protein is involved in signalling mediated through both FPR and CXCR, and the signalling cascades include a transient intracellular calcium increase, as well as downstream p38 MAPK and phosphoinositide 3-kinase activation. The data presented in this study provide support for two different signalling pathways to the neutrophil NADPH-oxidase, used by ligand binding to FPR/FPRL1 or CXCR, respectively.
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