دورية أكاديمية
Neutrophil GM-CSF receptor dynamics in acute lung injury.
العنوان: | Neutrophil GM-CSF receptor dynamics in acute lung injury. |
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المؤلفون: | De Alessandris S; Department of Medicine, University of Cambridge, Cambridge, United Kingdom., Ferguson GJ; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Dodd AJ; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Juss JK; Department of Medicine, University of Cambridge, Cambridge, United Kingdom., Devaprasad A; Department of Rheumatology and Clinical Immunology and Laboratory of Translational Immunology, University Medical Centre, Utrecht, Netherlands., Piper S; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Wyatt O; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Killick H; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Corkill DJ; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Cohen ES; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Pandit A; Department of Rheumatology and Clinical Immunology and Laboratory of Translational Immunology, University Medical Centre, Utrecht, Netherlands., Radstake TRDJ; Department of Rheumatology and Clinical Immunology and Laboratory of Translational Immunology, University Medical Centre, Utrecht, Netherlands., Simmonds R; Department of Medicine, University of Cambridge, Cambridge, United Kingdom., Condliffe AM; Department of Medicine, University of Cambridge, Cambridge, United Kingdom., Sleeman MA; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Cowburn AS; Department of Medicine, University of Cambridge, Cambridge, United Kingdom., Finch DK; Respiratory, Inflammation and Autoimmunity, MedImmune Ltd., Cambridge, United Kingdom., Chilvers ER; Department of Medicine, University of Cambridge, Cambridge, United Kingdom. |
المصدر: | Journal of leukocyte biology [J Leukoc Biol] 2019 Jun; Vol. 105 (6), pp. 1183-1194. Date of Electronic Publication: 2019 Apr 03. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Oxford University Press Country of Publication: England NLM ID: 8405628 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1938-3673 (Electronic) Linking ISSN: 07415400 NLM ISO Abbreviation: J Leukoc Biol Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 2023- : Oxford : Oxford University Press Original Publication: New York : Alan R. Liss, c1984- |
مواضيع طبية MeSH: | Acute Lung Injury/*immunology , Gene Expression Regulation/*immunology , Neutrophils/*immunology , Pulmonary Alveoli/*immunology , Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/*immunology, Acute Lung Injury/chemically induced ; Acute Lung Injury/genetics ; Acute Lung Injury/pathology ; Adult ; Animals ; Cell Line, Tumor ; Cytokine Receptor Common beta Subunit/genetics ; Cytokine Receptor Common beta Subunit/immunology ; Disease Models, Animal ; Female ; Humans ; Lipopolysaccharides/toxicity ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Transgenic ; Neutrophils/pathology ; Pulmonary Alveoli/pathology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Time Factors |
مستخلص: | GM-CSF is important in regulating acute, persistent neutrophilic inflammation in certain settings, including lung injury. Ligand binding induces rapid internalization of the GM-CSF receptor (GM-CSFRα) complex, a process essential for signaling. Whereas GM-CSF controls many aspects of neutrophil biology, regulation of GM-CSFRα expression is poorly understood, particularly the role of GM-CSFRα in ligand clearance and whether signaling is sustained despite major down-regulation of GM-CSFRα surface expression. We established a quantitative assay of GM-CSFRα surface expression and used this, together with selective anti-GM-CSFR antibodies, to define GM-CSFRα kinetics in human neutrophils, and in murine blood and alveolar neutrophils in a lung injury model. Despite rapid sustained ligand-induced GM-CSFRα loss from the neutrophil surface, which persisted even following ligand removal, pro-survival effects of GM-CSF required ongoing ligand-receptor interaction. Neutrophils recruited to the lungs following LPS challenge showed initially high mGM-CSFRα expression, which along with mGM-CSFRβ declined over 24 hr; this was associated with a transient increase in bronchoalveolar lavage fluid (BALF) mGM-CSF concentration. Treating mice in an LPS challenge model with CAM-3003, an anti-mGM-CSFRα mAb, inhibited inflammatory cell influx into the lung and maintained the level of BALF mGM-CSF. Consistent with neutrophil consumption of GM-CSF, human neutrophils depleted exogenous GM-CSF, independent of protease activity. These data show that loss of membrane GM-CSFRα following GM-CSF exposure does not preclude sustained GM-CSF/GM-CSFRα signaling and that this receptor plays a key role in ligand clearance. Hence neutrophilic activation via GM-CSFR may play an important role in neutrophilic lung inflammation even in the absence of high GM-CSF levels or GM-CSFRα expression. (©2018 The Authors. Society for Leukocyte Biology Published by Wiley Periodicals, Inc.) |
References: | N Engl J Med. 1992 Jul 2;327(1):28-35. (PMID: 1375975) Am J Respir Crit Care Med. 1997 Dec;156(6):1969-77. (PMID: 9412582) J Leukoc Biol. 2013 Sep;94(3):513-20. (PMID: 23794709) J Leukoc Biol. 2013 Jan;93(1):7-19. (PMID: 22904343) J Exp Med. 2008 Nov 24;205(12):2703-10. (PMID: 18955570) J Thorac Dis. 2014 Nov;6(11):1548-56. (PMID: 25478196) Blood. 1999 Mar 1;93(5):1579-85. (PMID: 10029586) J Infect Dis. 1999 Mar;179 Suppl 2:S342-52. (PMID: 10081506) J Exp Med. 1999 Sep 20;190(6):875-80. (PMID: 10499925) J Clin Invest. 1999 Apr;103(7):1015-21. (PMID: 10194474) Thorax. 2009 Aug;64(8):671-6. (PMID: 19213775) EMBO J. 1994 Nov 1;13(21):5176-85. (PMID: 7957082) Growth Factors. 1988;1(1):41-9. (PMID: 2483336) Crit Care Med. 2012 Jan;40(1):90-7. (PMID: 21926600) Pharm Res. 2015 Jan;32(1):286-99. (PMID: 25208874) J Immunol. 2003 Jun 1;170(11):5359-66. (PMID: 12759409) Am J Respir Cell Mol Biol. 2014 Feb;50(2):253-62. (PMID: 24010952) Am J Respir Crit Care Med. 2016 Oct 15;194(8):961-973. (PMID: 27064380) Am Rev Respir Dis. 1986 Feb;133(2):218-25. (PMID: 3004270) PLoS One. 2012;7(9):e45933. (PMID: 23029326) Am J Respir Cell Mol Biol. 2006 Jun;34(6):766-74. (PMID: 16474098) Blood. 1997 Oct 1;90(7):2772-83. (PMID: 9326245) Am J Respir Cell Mol Biol. 2011 Jun;44(6):879-87. (PMID: 20705940) Thorax. 2018 Oct;73(10):918-925. (PMID: 30064991) Am J Pathol. 1985 Apr;119(1):101-10. (PMID: 2984939) Eur J Immunol. 2004 Jun;34(6):1733-43. (PMID: 15162444) Antiviral Res. 2011 Nov;92(2):319-28. (PMID: 21925209) Am J Respir Crit Care Med. 2010 Nov 15;182(10):1292-304. (PMID: 20622029) Cytokine. 2008 Aug;43(2):114-23. (PMID: 18554923) Int Immunol. 1991 Jun;3(6):571-7. (PMID: 1832294) J Leukoc Biol. 2004 Feb;75(2):358-72. (PMID: 14634056) J Clin Invest. 2001 Dec;108(12):1797-806. (PMID: 11748263) Eur Respir J. 2011 Aug;38(2):285-94. (PMID: 21436349) Lancet Respir Med. 2013 Jul;1(5):395-401. (PMID: 24429204) Blood. 2002 Oct 1;100(7):2607-16. (PMID: 12239175) J Leukoc Biol. 2019 Jun;105(6):1183-1194. (PMID: 30942918) |
معلومات مُعتمدة: | United Kingdom WT_ Wellcome Trust |
فهرسة مساهمة: | Keywords: LPS; alveolar; apoptosis; inflammation; signaling |
المشرفين على المادة: | 0 (Csf2ra protein, mouse) 0 (Cytokine Receptor Common beta Subunit) 0 (GM-CSF receptor-alpha subunit, human) 0 (Lipopolysaccharides) 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor) |
تواريخ الأحداث: | Date Created: 20190404 Date Completed: 20200504 Latest Revision: 20210109 |
رمز التحديث: | 20231215 |
مُعرف محوري في PubMed: | PMC6850700 |
DOI: | 10.1002/JLB.3MA0918-347R |
PMID: | 30942918 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1938-3673 |
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DOI: | 10.1002/JLB.3MA0918-347R |