Activation of formyl peptide receptor 2 by WKYMVm enhances emergency granulopoiesis through phospholipase C activity
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Emergency granulopoiesis is a very important strategy to supply efficient neutrophil number in response to infection. However, molecular mechanism involved in this process remains unclear. Here, we found that administration of WKYMVm, an immune modulating peptide, to septic mice strongly increased neutrophil number through augmented emergency granulopoiesis. WKYMVm-induced emergency granulopoiesis was blocked not only by a formyl peptide receptor 2 (FPR2) antagonist (WRW4), but also by FPR2 deficiency. As progenitors of neutrophils, Lin−c-kit＋Sca-1− cells expressed FPR2. WKYMVm-induced emergency granulopoiesis was also blocked by a phospholipase C inhibitor (U-73122). These results suggest that WKYMVm can stimulate emergency granulopoiesis via FPR2 and phospholipase C enzymatic activity.
Abstract
Emergency granulopoiesis is a very important strategy to supply efficient neutrophil number in response to infection. However, molecular mechanism involved in this process remains unclear. Here, we found that administration of WKYMVm, an immune modulating peptide, to septic mice strongly increased neutrophil number through augmented emergency granulopoiesis. WKYMVm-induced emergency granulopoiesis was blocked not only by a formyl peptide receptor 2 (FPR2) antagonist (WRW4), but also by FPR2 deficiency. As progenitors of neutrophils, Lin−c-kit＋Sca-1− cells expressed FPR2. WKYMVm-induced emergency granulopoiesis was also blocked by a phospholipase C inhibitor (U-73122). These results suggest that WKYMVm can stimulate emergency granulopoiesis via FPR2 and phospholipase C enzymatic activity.
참고문헌 (27)
- Smith JA, "Neutrophils, host defense, and inflammation: a double-edged sword", J Leukoc Biol, 56, pp.672~686 (1994)[DOI]
- Kruger P, "Neutrophils: Between host defence, immune modulation, and tissue injury", PLoS Pathog, 11, pp.e1004651~ (2015)[DOI]
- DeCoursey TE, "The intimate and controversial relationship between voltage-gated proton channels and the phagocyte NADPH oxidase", Immunol Rev, 273, pp.194~218 (2016)[DOI]
- Iwasaki H, "Myeloid lineage commitment from the hematopoietic stem cell", Immunity, 22, pp.726~740 (2007)
- Seita J, "Hematopoietic stem cell: self-renewal versus differentiation", Wiley Interdiscip Rev Syst Biol Med, 2, pp.640~653 (2010)[DOI]
- Manz MG, "Emergency granulopoiesis", Nat Rev Immunol, 14, pp.302~314 (2014)[DOI]
- Seo JK, "A peptide with unique receptor specificity: stimulation of phosphoinositide hydrolysis and induction of superoxide generation in human neutrophils", J Immunol, 158, pp.1895~1901 (1997)
- Bae YS, "Trp-Lys-Tyr-Met-Val-D-Met stimulates superoxide generation and killing of Staphylococcus aureus via phospholipase D activation in human monocytes", J Leukoc Biol, 65, pp.241~248 (1999)[DOI]
- Bae YS, "Independent functioning of cytosolic phospholipase A2 and phospholipase D1 in Trp-Lys-Tyr-Met-Val-D-Met-induced superoxide generation in human monocytes", J Immunol, 164, pp.4089~4096 (2000)[DOI]
- Schepetkin IA, "Identification of novel formyl peptide receptor-like 1 agonists that induce macrophage tumor necrosis factor <TEX>${\alpha}$<", TEX> Production, 2008, pp.74, 392~402
- Le Y, "Utilization of two seven-transmembrane, G protein-coupled receptors, formyl peptide receptor-like 1 and formyl peptide receptor, by the synthetic hexapeptide WKYMVm for human phagocyte activation", J Immunol, 163, pp.6777~6784 (1999)
- Bae YS, "Differential activation of formyl peptide receptor signaling by peptide ligands", Mol Pharmacol, 64, pp.841~847 (2003)[DOI]
- Kim SD, "The agonists of formyl peptide receptors prevent development of severe sepsis after microbial infection", J Immunol, 185, pp.4302~4310 (2010)[DOI]
- Noh DY, "Phosphoinositidespecific phospholipase C and mitogenic signaling", Biochim Biophys Acta, 1242, pp.99~113 (1995)
- 서판길, "Multiple roles of phosphoinositide-specific phospholipase C isozymes", BMB reports, 41(6), pp.415~434 (2008), 한국생화학분자생물학회
- Lattanzio R, "Role of phospholipase C in cell invasion and metastasis", Adv Biol Regul, 53, pp.309~318 (2013)[DOI]
- Cheng M, "Targeting phospholipid Metabolism in cancer", Front Oncol, 6, pp.266~ (2016)
- Sonego F, "Paradoxical roles of the neutrophil in sepsis: protective and deleterious", Front Immunol, 7, pp.155~ (2016)
- Bae YS, "Identification of peptides that antagonize formyl peptide receptor-like 1-mediated signaling", J Immunol, 173, pp.607~614 (2004)[DOI]
- Kwak HJ, "Myeloid cell-derived reactive oxygen species externally regulate the proliferation of myeloid progenitors in emergency granulopoiesis", Immunity, 42, pp.159~171 (2015)[DOI]
- Ye RD, "International union of basic and clinical pharmacology. LXXIII. nomenclature for the formyl peptide receptor (FPR) family", Pharmacol Rev, 61, pp.119~161 (2009)[DOI]
- Lee HY, "Formyl peptide receptors in cellular differentiation and inflammatory diseases", J Cell Biochem, 6, pp.1300~1307 (2017)
- Rhee SG, "Regulation of phosphoinositide-specific phospholipase C", Annu Rev Biochem, 70, pp.281~312 (2001)[DOI]
- Zhang S, "A C-terminal mutant of the G protein beta subunit deficient in the activation of phospholipase C-beta", J Biol Chem, 271, pp.20208~20212 (1996)[DOI]
- Park MY, "FAM19A5, a brain-specific chemokine, inhibits RANKL-induced osteoclast formation through Formyl peptide receptor 2", Sci Rep, 7, pp.15575~ (2017)[DOI]
- Lee SK, "Phospholipase D2 drives mortality in sepsis by inhibiting neutrophil extracellular trap formation and down-regulating CXCR2", J Exp Med, 212, pp.1381~1390 (2015)[DOI]
- Kim SD, "Activation of CXCR2 by extracellular matrix degradation product acetylated Pro-Gly-Pro has therapeutic effects against sepsis", Am J Respir Crit Care Med, 184, pp.243~251 (2011)[DOI]