{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T20:39:21Z","timestamp":1783370361830,"version":"3.54.6"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2022,7,1]],"date-time":"2022-07-01T00:00:00Z","timestamp":1656633600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100012891","name":"Medical Research Charities Group\/Health Research Board Ireland","doi-asserted-by":"publisher","award":["MRCG-2018-04"],"award-info":[{"award-number":["MRCG-2018-04"]}],"id":[{"id":"10.13039\/100012891","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001448","name":"US Alpha-1 Foundation","doi-asserted-by":"crossref","award":["2018"],"award-info":[{"award-number":["2018"]}],"id":[{"id":"10.13039\/100001448","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Medical Research Charities Group\/Health Research Board Ireland","award":["MRCG-2018-04"],"award-info":[{"award-number":["MRCG-2018-04"]}]},{"DOI":"10.13039\/100001448","name":"US Alpha-1 Foundation","doi-asserted-by":"crossref","award":["2018"],"award-info":[{"award-number":["2018"]}],"id":[{"id":"10.13039\/100001448","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Alpha-1 antitrypsin deficiency (AATD) is characterized by neutrophil-dominated inflammation resulting in emphysema. The cholesterol-rich neutrophil outer plasma membrane plays a central role in adhesion and subsequent transmigration to underlying tissues. This study aimed to investigate mechanisms of increased neutrophil adhesion in AATD and whether alpha-1 antitrypsin (AAT) augmentation therapy abrogates this effect. Plasma and blood neutrophils were donated by healthy controls (n\u2009=\u200920), AATD (n\u2009=\u200930), and AATD patients after AAT augmentation therapy (n\u2009=\u20096). Neutrophil membrane protein expression was investigated using liquid chromatography\u2013tandem mass spectrometry. The effect of once-weekly intravenous AAT augmentation therapy was assessed by calcium fluorometric, \u03bc-calpain, and cell adhesion assays. Decreased neutrophil plasma membrane cholesterol content (P\u2009=\u20090.03), yet increased abundance of integrin \u03b1-M (fold change 1.91), integrin \u03b1-L (fold change 3.76), and cytoskeletal adaptor proteins including talin-1 (fold change 4.04) were detected on AATD neutrophil plasma membrane fractions. The described inflammatory induced structural changes were a result of a more than twofold increased cytosolic calcium concentration (P\u2009=\u20090.02), leading to significant calcium-dependent \u03bc-calpain activity (3.5-fold change; P\u2009=\u20090.005), resulting in proteolysis of the membrane cholesterol trafficking protein caveolin-1. Treatment of AAT-deficient individuals with AAT augmentation therapy resulted in increased caveolin-1 and membrane cholesterol content (111.8\u2009\u00b1\u200915.5 vs. 64.18\u2009\u00b1\u20097.8 \u03bcg\/2\u2009\u00d7\u2009107 cells before and after treatment, respectively; P\u2009=\u20090.02), with concurrent decreased neutrophil integrin expression and adhesion. Results demonstrate an auxiliary benefit of AAT augmentation therapy, evident by a decrease in circulating inflammation and controlled neutrophil adhesion.<\/jats:p>","DOI":"10.1165\/rcmb.2021-0433oc","type":"journal-article","created":{"date-parts":[[2022,5,4]],"date-time":"2022-05-04T15:07:00Z","timestamp":1651676820000},"page":"76-88","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":13,"title":["Alpha-1 Antitrypsin Therapy Modifies Neutrophil Adhesion in Patients with Obstructive Lung Disease"],"prefix":"10.1093","volume":"67","author":[{"given":"Tom","family":"McEnery","sequence":"first","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle M.","family":"White","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Debananda","family":"Gogoi","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Orla","family":"Coleman","sequence":"additional","affiliation":[{"name":"National Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Bergin","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bakr","family":"Jundi","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan","family":"Flannery","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"},{"name":"Col\u00e1iste Dh\u00falaigh College of Further Education, Dublin 17, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fatima Abbas T.","family":"Alsaif","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah A.","family":"Landers","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2821-6861","authenticated-orcid":false,"given":"Michelle","family":"Casey","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danielle","family":"Dunlea","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paula","family":"Meleady","sequence":"additional","affiliation":[{"name":"National Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Noel G.","family":"McElvaney","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1922-0447","authenticated-orcid":false,"given":"Emer P.","family":"Reeves","sequence":"additional","affiliation":[{"name":"Irish Centre for Genetic Lung Disease, Royal College of Surgeons in Ireland, Dublin 9, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2022,7,1]]},"reference":[{"key":"2026012203592524500_bib1","doi-asserted-by":"crossref","first-page":"2101410","DOI":"10.1183\/13993003.01410-2021","article-title":"Alpha-1 antitrypsin deficiency: clarifying the role of the putative protective threshold","volume":"59","author":"Franciosi","year":"2022","journal-title":"Eur Respir J"},{"key":"2026012203592524500_bib2","doi-asserted-by":"crossref","first-page":"419","DOI":"10.1164\/rccm.201311-1984OC","article-title":"Clarification of the risk of chronic obstructive pulmonary disease in \u03b11-antitrypsin deficiency PiMZ heterozygotes","volume":"189","author":"Molloy","year":"2014","journal-title":"Am J Respir Crit Care Med"},{"key":"2026012203592524500_bib3","article-title":"Alpha-1 antitrypsin deficiency-associated panniculitis","author":"Franciosi","year":"2021","journal-title":"J Am Acad Dermatol"},{"key":"2026012203592524500_bib4","doi-asserted-by":"crossref","first-page":"16051","DOI":"10.1038\/nrdp.2016.51","article-title":"\u03b11-Antitrypsin deficiency","volume":"2","author":"Greene","year":"2016","journal-title":"Nat Rev Dis Primers"},{"key":"2026012203592524500_bib5","doi-asserted-by":"crossref","first-page":"360","DOI":"10.1016\/S0140-6736(15)60860-1","article-title":"Intravenous augmentation treatment and lung density in severe \u03b11 antitrypsin deficiency (RAPID): a randomised, double-blind, placebo-controlled trial","volume":"386","author":"Chapman","year":"2015","journal-title":"Lancet"},{"key":"2026012203592524500_bib6","doi-asserted-by":"crossref","first-page":"891","DOI":"10.1172\/JCI115391","article-title":"Neutrophil accumulation in the lung in alpha 1-antitrypsin deficiency. 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