scholarly journals Synthesis, biological evaluation, molecular modeling, and structural analysis of new pyrazole and pyrazolone derivatives as N‐formyl peptide receptors (FPRs) agonists

2021 ◽  
Author(s):  
Claudia Vergelli ◽  
Andrei I. Khlebnikov ◽  
Letizia Crocetti ◽  
Gabriella Guerrini ◽  
Niccolò Cantini ◽  
...  
Keyword(s):  
Molecular Modeling ◽  
Structural Analysis ◽  
Biological Evaluation ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Pyrazolone Derivatives ◽  
Formyl Peptide

The Role of Formyl Peptide Receptors in Microbial Infection and Inflammation

2003 ◽  
Vol 2 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Yingying Le ◽  
Ronghua Sun ◽  
Guoguang Ying ◽  
Pablo Iribarren ◽  
Ji Wang
Keyword(s):  
Microbial Infection ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Infection And Inflammation

scholarly journals G-protein–coupled formyl peptide receptors play a dual role in neutrophil chemotaxis and bacterial phagocytosis

2019 ◽  
Vol 30 (3) ◽  
pp. 346-356 ◽  
Author(s):  
Xi Wen ◽  
Xuehua Xu ◽  
Wenxiang Sun ◽  
Keqiang Chen ◽  
Miao Pan ◽  
...  
Keyword(s):  
G Protein ◽  
Receptor Tyrosine Kinase ◽  
Tyrosine Kinases ◽  
Actin Polymerization ◽  
G Protein Coupled Receptors ◽  
Peptide Receptors ◽  
Tyrosine Kinase Signaling ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
G Protein Coupled

A dogma of innate immunity is that neutrophils use G-protein–coupled receptors (GPCRs) for chemoattractant to chase bacteria through chemotaxis and then use phagocytic receptors coupled with tyrosine kinases to destroy opsonized bacteria via phagocytosis. Our current work showed that G-protein–coupled formyl peptide receptors (FPRs) directly mediate neutrophil phagocytosis. Mouse neutrophils lacking formyl peptide receptors (Fpr1/2–/–) are defective in the phagocytosis of Escherichia coli and the chemoattractant N-formyl-Met-Leu-Phe (fMLP)-coated beads. fMLP immobilized onto the surface of a bead interacts with FPRs, which trigger a Ca2+response and induce actin polymerization to form a phagocytic cup for engulfment of the bead. This chemoattractant GPCR/Gi signaling works independently of phagocytic receptor/tyrosine kinase signaling to promote phagocytosis. Thus, in addition to phagocytic receptor-mediated phagocytosis, neutrophils also utilize the chemoattractant GPCR/Gi signaling to mediate phagocytosis to fight against invading bacteria.

Formyl-Peptide Receptors in Infection, Inflammation, and Cancer

2018 ◽  
Vol 39 (10) ◽  
pp. 815-829 ◽  
Author(s):  
Elisabeth Weiß ◽  
Dorothee Kretschmer
Keyword(s):  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide

scholarly journals Formyl-Peptide Receptor Activation Enhances Phagocytosis of Community-Acquired Methicillin-Resistant Staphylococcus aureus

2019 ◽  
Author(s):  
Elisabeth Weiß ◽  
Katja Schlatterer ◽  
Christian Beck ◽  
Andreas Peschel ◽  
Dorothee Kretschmer
Keyword(s):  
Staphylococcus Aureus ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Receptor Activation ◽  
Formyl Peptide Receptor ◽  
Peptide Receptors ◽  
Highly Pathogenic ◽  
Methicillin Resistant ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
First Time

Abstract Background Formyl-peptide receptors (FPRs) are important pattern recognition receptors that sense specific bacterial peptides. Formyl-peptide receptors are highly expressed on neutrophils and monocytes, and their activation promotes the migration of phagocytes to sites of infection. It is currently unknown whether FPRs may also influence subsequent processes such as bacterial phagocytosis and killing. Staphylococcus aureus, especially highly pathogenic community-acquired methicillin-resistant S aureus strains, release high amounts of FPR2 ligands, the phenol-soluble modulins. Methods We demonstrate that FPR activation leads to upregulation of complement receptors 1 and 3 as well as FCγ receptor I on neutrophils and, consequently, increased opsonic phagocytosis of S aureus and other pathogens. Results Increased phagocytosis promotes killing of S aureus and interleukin-8 release by neutrophils. Conclusions We show here for the first time that FPRs govern opsonic phagocytosis. Manipulation of FPR2 activation could open new therapeutic opportunities against bacterial pathogens.

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