{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T01:01:54Z","timestamp":1791248514976,"version":"4.1.0"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2012,8,1]],"date-time":"2012-08-01T00:00:00Z","timestamp":1343779200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>COPD is a complex disease with heterogeneous manifestations. Attempts have been made to define different phenotypes that could guide toward better disease understanding. We described before that smokers can develop either panlobular (PLE) or centrilobular emphysema (CLE). The latter has worse small airways remodeling and narrowing, which account for the airflow obstruction similar to asthma.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Because of the small airways involvement in CLE similar to asthma, we hypothesized a role for mast cells in CLE but not in PLE. Hence, we investigated mast cell infiltration, along with overall inflammation, and their relation with hyperreactivity and emphysema type in COPD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We studied lung function, emphysema type, mast cells, and overall inflammation in small airways and alveolar walls, along with alveolar wall thickening in 67 subjects undergoing lung resection (59 smokers, 8 nonsmokers).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Twenty-seven smokers had CLE, 24 had PLE, and 8 had no emphysema. Mast cells were significantly increased in CLE compared with PLE and control subjects. Especially relevant was the mast cell increase in airway smooth muscle in CLE, which related significantly to airway hyperreactivity. CD4+T cells, neutrophils, and macrophages, but not eosinophils and CD8+T cells, were significantly higher in CLE than PLE. Alveolar wall thickness was increased in all smokers, but significantly more in CLE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The pathological phenotypes of COPD CLE and PLE show important differences in their overall inflammation with a protagonism of mast cells, which are related to airway reactivity. These findings highlight the distinctness of these COPD phenotypes and the role of mast cells in the pathophysiology of COPD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.201112-2142oc","type":"journal-article","created":{"date-parts":[[2012,6,8]],"date-time":"2012-06-08T00:39:57Z","timestamp":1339115997000},"page":"233-239","source":"Crossref","is-referenced-by-count":57,"title":["Mast Cell Infiltration Discriminates between Histopathological Phenotypes of Chronic Obstructive Pulmonary Disease"],"prefix":"10.1093","volume":"186","author":[{"given":"Andrea","family":"Ballarin","sequence":"first","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erica","family":"Bazzan","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rafael Hernandez","family":"Zenteno","sequence":"additional","affiliation":[{"name":"Departamento de Investigacion en Tabaquismo, Istituto Nacional de Enfermedades Respiratorias, Ciudad de Mexico, Mexico"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Graziella","family":"Turato","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simonetta","family":"Baraldo","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dora","family":"Zanovello","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Mutti","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James C.","family":"Hogg","sequence":"additional","affiliation":[{"name":"James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia and St Paul\u2019s Hospital, Vancouver, Canada; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marina","family":"Saetta","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel G.","family":"Cosio","sequence":"additional","affiliation":[{"name":"Department of Cardiac, Thoracic, and Vascular Sciences, University of Padova, Padova, Italy"},{"name":"Respiratory Division, Meakins-Christie Laboratories, McGill University, Montreal, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,8,1]]},"reference":[{"key":"2026032101001578400_bib1","doi-asserted-by":"crossref","first-page":"598","DOI":"10.1164\/rccm.200912-1843CC","article-title":"Chronic obstructive pulmonary disease phenotypes: the future of COPD","volume":"182","author":"Han","year":"2010","journal-title":"Am J Respir Crit Care Med"},{"key":"2026032101001578400_bib2","doi-asserted-by":"crossref","first-page":"231","DOI":"10.1111\/j.1365-2818.1949.tb00981.x","article-title":"The use of thin sections of entire organs in morbid anatomical studies","volume":"69","author":"Gough","year":"1949","journal-title":"J R Microsc Soc"},{"key":"2026032101001578400_bib3","doi-asserted-by":"crossref","first-page":"219","DOI":"10.1136\/thx.12.3.219","article-title":"The centrilobular form of hypertrophic emphysema and its relation to chronic bronchitis","volume":"12","author":"Leopold","year":"1957","journal-title":"Thorax"},{"key":"2026032101001578400_bib4","doi-asserted-by":"crossref","first-page":"277","DOI":"10.1016\/0002-9343(60)90024-3","article-title":"Correlation of lung macrosections with pulmonary function in emphysema","volume":"29","author":"Sweet","year":"1960","journal-title":"Am J Med"},{"key":"2026032101001578400_bib5","doi-asserted-by":"crossref","first-page":"547","DOI":"10.1136\/thx.28.5.547","article-title":"Centrilobular emphysema and panlobular emphysema: two different diseases","volume":"28","author":"Anderson","year":"1973","journal-title":"Thorax"},{"key":"2026032101001578400_bib6","doi-asserted-by":"crossref","first-page":"1385","DOI":"10.1164\/ajrccm\/144.6.1385","article-title":"Centrilobular and panlobular emphysema in smokers. 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