BACKGROUND: Epidermal growth factor (EGF)-like module-containing mucin-like hormone receptor-like 2 (EMR2) is an adhesion G protein-coupled receptor previously shown to potentiate neutrophil responses to a number of inflammatory stimuli. EMR2 activation promotes neutrophil adhesion and migration, and augments production of reactive oxygen species and degranulation. In this study, we examined the effect of EMR2 ligation by its specific antibody on the cytokine expression profile and cell survival of lipopolysaccharide (LPS)-treated neutrophils. METHODS: Neutrophils were treated with LPS in the absence or presence of the anti-EMR2 mAb, 2A1. Cell apoptosis was determined by flow cytometry analysis using annexin-V and propidium iodide staining. Cell supernatants were collected for the detection of cytokine secretion by enzyme-linked immunosorbent assay. RESULTS: We confirmed the specific priming effect of EMR2 on the response of neutrophils to formyl-Met-Leu-Phe by measuring the production of reactive oxygen species. Furthermore, we showed that EMR2 ligation suppresses LPS-induced neutrophil survival. In addition, we demonstrated that ligation of EMR2 changes the secretion profiles of multiple cytokines, including interleukin (IL)-6, IL-8, and monocyte chemotactic protein-1. Finally, higher levels of EMR2 were detected on neutrophils of liver cirrhosis patients and were correlated to a pro-apoptotic phenotype. CONCLUSION: Collectively, the present data indicate a functional role for EMR2 in the modulation of neutrophil activation during inflammation.
BACKGROUND:Epidermal growth factor (EGF)-like module-containing mucin-like hormone receptor-like 2 (EMR2) is an adhesion G protein-coupled receptor previously shown to potentiate neutrophil responses to a number of inflammatory stimuli. EMR2 activation promotes neutrophil adhesion and migration, and augments production of reactive oxygen species and degranulation. In this study, we examined the effect of EMR2 ligation by its specific antibody on the cytokine expression profile and cell survival of lipopolysaccharide (LPS)-treated neutrophils. METHODS: Neutrophils were treated with LPS in the absence or presence of the anti-EMR2 mAb, 2A1. Cell apoptosis was determined by flow cytometry analysis using annexin-V and propidium iodide staining. Cell supernatants were collected for the detection of cytokine secretion by enzyme-linked immunosorbent assay. RESULTS: We confirmed the specific priming effect of EMR2 on the response of neutrophils to formyl-Met-Leu-Phe by measuring the production of reactive oxygen species. Furthermore, we showed that EMR2 ligation suppresses LPS-induced neutrophil survival. In addition, we demonstrated that ligation of EMR2 changes the secretion profiles of multiple cytokines, including interleukin (IL)-6, IL-8, and monocyte chemotactic protein-1. Finally, higher levels of EMR2 were detected on neutrophils of liver cirrhosispatients and were correlated to a pro-apoptotic phenotype. CONCLUSION: Collectively, the present data indicate a functional role for EMR2 in the modulation of neutrophil activation during inflammation.
Authors: S M Lewis; D F Treacher; J Edgeworth; G Mahalingam; C S Brown; T A Mare; M Stacey; R Beale; K A Brown Journal: Clin Exp Immunol Date: 2015-09-22 Impact factor: 4.330
Authors: Andrea N Naranjo; Geethani Bandara; Yun Bai; Margery G Smelkinson; Araceli Tobío; Hirsh D Komarow; Steven E Boyden; Daniel L Kastner; Dean D Metcalfe; Ana Olivera Journal: J Invest Dermatol Date: 2020-03-25 Impact factor: 8.551
Authors: Steven E Boyden; Avanti Desai; Glenn Cruse; Michael L Young; Hyejeong C Bolan; Linda M Scott; A Robin Eisch; R Daniel Long; Chyi-Chia R Lee; Colleen L Satorius; Andrew J Pakstis; Ana Olivera; James C Mullikin; Eliane Chouery; André Mégarbané; Myrna Medlej-Hashim; Kenneth K Kidd; Daniel L Kastner; Dean D Metcalfe; Hirsh D Komarow Journal: N Engl J Med Date: 2016-02-03 Impact factor: 91.245
Authors: Michael Safaee; Michael E Ivan; Michael C Oh; Taemin Oh; Eli T Sayegh; Gurvinder Kaur; Matthew Z Sun; Orin Bloch; Andrew T Parsa Journal: Oncol Rev Date: 2014-04-01