MAP kinases in regulation of NOX activity stimulated through two types of formyl peptide receptors in murine bone marrow granulocytes

2021 ◽  
pp. 110205
Author(s):  
Yu.V. Filina ◽  
A.G. Gabdoulkhakova ◽  
A.A. Rizvanov ◽  
V.G. Safronova
Keyword(s):  
Bone Marrow ◽  
Map Kinases ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Murine Bone Marrow ◽  
Formyl Peptide ◽  
Bone Marrow Granulocytes

scholarly journals Crotoxin Isolated fromCrotalus durissus terrificusVenom Modulates the Functional Activity of Dendritic Cells via Formyl Peptide Receptors

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
A. P. Freitas ◽  
B. C. Favoretto ◽  
P. B. Clissa ◽  
S. C. Sampaio ◽  
E. L. Faquim-Mauro
Keyword(s):  
Dendritic Cells ◽  
Functional Activity ◽  
Mapk Signaling ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Murine Bone Marrow ◽  
Mhc Ii ◽  
Formyl Peptide ◽  
Crotalus Durissus ◽  
Mapk Signaling Pathways

TheCrotalus durissus terrificusrattlesnake venom, its main toxin, crotoxin (CTX), and its crotapotin (CA) and phospholipase A2(CB) subunits modulate the immune system. Formyl peptide receptors (FPRs) and lipoxin A4(LXA4) are involved in CTX’s effect on macrophages and neutrophils. Dendritic cells (DCs) are plasticity cells involved in the induction of adaptive immunity and tolerance maintenance. Therefore, we evaluated the effect of CTX, CA or CB on the maturation of DCs derived from murine bone marrow (BM). According to data, CTX and CB—but not CA—induced an increase of MHC-II, but not costimulatory molecules on DCs. Furthermore, CTX and CB inhibited the expression of costimulatory and MHC-II molecules, secretion of proinflammatory cytokines and NF-κBp65 and p38/ERK1/2-MAPK signaling pathways by LPS-incubated DCs. Differently, CTX and CB induced IL-10, PGE2and LXA4secretion in LPS-incubated DCs. Lower proliferation and IL-2 secretion were verified in coculture of CD3+cells and DCs incubated with LPS plus CTX or CB compared with LPS-incubated DCs. The effect of CTX and CB on DCs was abolished in cultures incubated with a FPRs antagonist. Hence, CTX and CB exert a modulation on functional activity of DCs; we also checked the involvement the FPR family on cell activities.

scholarly journals Functional Expression ofN-Formyl Peptide Receptors in Human Bone Marrow-Derived Mesenchymal Stem Cells

Stem Cells ◽  
2007 ◽  
Vol 25 (5) ◽  
pp. 1263-1269 ◽  
Author(s):  
Anand Viswanathan ◽  
Richard G. Painter ◽  
Nicholas A. Lanson ◽  
Guoshun Wang
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Functional Expression ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
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.

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