The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals

Danielle M Dunlea, Laura T Fee, Thomas McEnery, Noel G McElvaney, Emer P Reeves Irish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland Abstract: Alpha-1 antitrypsin (AAT) is the most abundant serine protease inhibitor c...

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Autores principales: Dunlea DM, Fee LT, McEnery T, McElvaney NG, Reeves EP
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Lenguaje:EN
Publicado: Dove Medical Press 2018
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Acceso en línea:https://doaj.org/article/f1620ab2eb794c16b3c4e4484422dd48
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spelling oai:doaj.org-article:f1620ab2eb794c16b3c4e4484422dd482021-12-02T04:53:09ZThe impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals1178-7031https://doaj.org/article/f1620ab2eb794c16b3c4e4484422dd482018-03-01T00:00:00Zhttps://www.dovepress.com/the-impact-of-alpha-1-antitrypsin-augmentation-therapy-on-neutrophil-d-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Danielle M Dunlea, Laura T Fee, Thomas McEnery, Noel G McElvaney, Emer P Reeves Irish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland Abstract: Alpha-1 antitrypsin (AAT) is the most abundant serine protease inhibitor circulating in the blood. AAT deficiency (AATD) is an autosomal codominant condition affecting an estimated 3.4 million individuals worldwide. The clinical disease associated with AATD can present in a number of ways including COPD, liver disease, panniculitis and antineutrophil cytoplasmic antibody vasculitis. AATD is the only proven genetic risk factor for the development of COPD, and deficient individuals who smoke are disposed to more aggressive disease. Principally, AAT is a serine protease inhibitor; however, over the past number of years, the assessment of AAT as simply an antiprotease has evolved, and it is now recognized that AAT has significant anti-inflammatory properties affecting a wide range of cells, including the circulating neutrophil. Keywords: neutrophils, alpha-1 antitrypsin deficiency, alpha-1 antitrypsin augmentation, inflammation, airways diseaseDunlea DMFee LTMcEnery TMcElvaney NGReeves EPDove Medical PressarticleNeutrophilsalpha-1 antitrypsin deficiencyalpha-1 antitrypsin augmentationinflammationairways diseasePathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 11, Pp 123-134 (2018)
institution DOAJ
collection DOAJ
language EN
topic Neutrophils
alpha-1 antitrypsin deficiency
alpha-1 antitrypsin augmentation
inflammation
airways disease
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
spellingShingle Neutrophils
alpha-1 antitrypsin deficiency
alpha-1 antitrypsin augmentation
inflammation
airways disease
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
Dunlea DM
Fee LT
McEnery T
McElvaney NG
Reeves EP
The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
description Danielle M Dunlea, Laura T Fee, Thomas McEnery, Noel G McElvaney, Emer P Reeves Irish Centre for Genetic Lung Disease, Department of Medicine, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland Abstract: Alpha-1 antitrypsin (AAT) is the most abundant serine protease inhibitor circulating in the blood. AAT deficiency (AATD) is an autosomal codominant condition affecting an estimated 3.4 million individuals worldwide. The clinical disease associated with AATD can present in a number of ways including COPD, liver disease, panniculitis and antineutrophil cytoplasmic antibody vasculitis. AATD is the only proven genetic risk factor for the development of COPD, and deficient individuals who smoke are disposed to more aggressive disease. Principally, AAT is a serine protease inhibitor; however, over the past number of years, the assessment of AAT as simply an antiprotease has evolved, and it is now recognized that AAT has significant anti-inflammatory properties affecting a wide range of cells, including the circulating neutrophil. Keywords: neutrophils, alpha-1 antitrypsin deficiency, alpha-1 antitrypsin augmentation, inflammation, airways disease
format article
author Dunlea DM
Fee LT
McEnery T
McElvaney NG
Reeves EP
author_facet Dunlea DM
Fee LT
McEnery T
McElvaney NG
Reeves EP
author_sort Dunlea DM
title The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
title_short The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
title_full The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
title_fullStr The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
title_full_unstemmed The impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
title_sort impact of alpha-1 antitrypsin augmentation therapy on neutrophil-driven respiratory disease in deficient individuals
publisher Dove Medical Press
publishDate 2018
url https://doaj.org/article/f1620ab2eb794c16b3c4e4484422dd48
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