Structural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthma

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorROSSI, Renata Calciolari
dc.contributor.authorANONNI, Raquel
dc.contributor.authorFERREIRA, Diogenes Seraphim
dc.contributor.authorSILVA, Luiz Fernando Ferraz da
dc.contributor.authorMAUAD, Thais
dc.date.accessioned2019-09-23T14:20:30Z
dc.date.available2019-09-23T14:20:30Z
dc.date.issued2019
dc.description.abstractBackground There is interest in better understanding vessel pathology in asthma, given the findings of loss of peripheral vasculature associated with disease severity by imaging and altered markers of endothelial activation. To date, vascular changes in asthma have been described mainly at the submucosal capillary level of the bronchial microcirculation, with sparse information available on the pathology of bronchial and pulmonary arteries. The aim of this study was to describe structural and endothelial activation markers in bronchial arteries (BAs) and pulmonary arteries (PAs) of asthma patients who died during a fatal asthma attack. Methods Autopsy lung tissue was obtained from 21 smoking and non-smoking patients who died of an asthma attack and nine non-smoking control patients. Verhoeff-Masson trichrome staining was used to analyse the structure of arteries. Using immuno-histochemistry and image analyses, we quantified extracellular matrix (ECM) components (collagen I, collagen III, versican, tenascin, fibronectin, elastic fibres), adhesion molecules [vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1)] and markers of vascular tone/dysfunction [endothelin-1 (ET-1) and angiotensin II type 2 receptor (AT2)] in PAs and BAs. Results There were no significant differences in ECM components, ICAM-1, ET-1 or AT2 between asthma patients and controls. Smoking asthma patients presented with decreased content of collagen III in both BA (p = 0.046) and PA (p = 0.010) walls compared to non-smoking asthma patients. Asthma patients had increased VCAM-1 content in the BA wall (p = 0.026) but not in the PA wall. Conclusion Our data suggest that the mechanisms linking asthma and arterial functional abnormalities might involve systemic rather than local mediators. Loss of collagen III in the PA was observed in smoking asthma patients, and this was compatible with the degradative environment induced by cigarette smoking. Our data also reinforce the idea that the mechanisms of leukocyte efflux via adhesion molecules differ between bronchial and pulmonary circulation, which might be relevant to understanding and treating the distal lung in asthma.eng
dc.description.indexPubMedeng
dc.description.sponsorshipBrazilian Research Council (CNPq) - Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [305428/2014-4]
dc.identifier.citationALLERGY ASTHMA AND CLINICAL IMMUNOLOGY, v.15, n.1, article ID 50, 9p, 2019
dc.identifier.doi10.1186/s13223-019-0363-0
dc.identifier.issn1710-1492
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/33565
dc.language.isoeng
dc.publisherBMCeng
dc.relation.ispartofAllergy Asthma and Clinical Immunology
dc.rightsopenAccesseng
dc.rights.holderCopyright BMCeng
dc.subjectAsthmaeng
dc.subjectPulmonary arteryeng
dc.subjectBronchial arteryeng
dc.subjectPathologyeng
dc.subjectExtracellular matrixeng
dc.subjectAdhesion moleculeseng
dc.subjectEndothelial activationeng
dc.subjectRemodellingeng
dc.subject.otherairway inflammationeng
dc.subject.otherlungeng
dc.subject.otherreceptoreng
dc.subject.otherdiseaseeng
dc.subject.otherexpressioneng
dc.subject.wosAllergyeng
dc.subject.wosImmunologyeng
dc.titleStructural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthmaeng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.author.externalROSSI, Renata Calciolari:Univ Sao Paulo, Sch Med, Dept Pathol, Ave Dr Arnaldo 455, BR-01246903 Sao Paulo, SP, Brazil; Univ Oeste Paulista, Dept Pathol, Presidente Prudente, SP, Brazil
hcfmusp.author.externalANONNI, Raquel:Univ Sao Paulo, Sch Med, Dept Pathol, Ave Dr Arnaldo 455, BR-01246903 Sao Paulo, SP, Brazil; Univ Fed Triangulo Mineiro, Dept Physiotherapy, Uberaba, MG, Brazil
hcfmusp.author.externalFERREIRA, Diogenes Seraphim:Univ Sao Paulo, Sch Med, Dept Pathol, Ave Dr Arnaldo 455, BR-01246903 Sao Paulo, SP, Brazil; Univ Fed Parana, Hosp Clin, Allergy & Immunol, Curitiba, Parana, Brazil
hcfmusp.citation.scopus6
hcfmusp.contributor.author-fmusphcLUIZ FERNANDO FERRAZ DA SILVA
hcfmusp.contributor.author-fmusphcTHAIS MAUAD
hcfmusp.description.articlenumber50
hcfmusp.description.issue1
hcfmusp.description.volume15
hcfmusp.origemWOS
hcfmusp.origem.pubmed31485240
hcfmusp.origem.scopus2-s2.0-85071652351
hcfmusp.origem.wosWOS:000483502600002
hcfmusp.publisher.cityLONDONeng
hcfmusp.publisher.countryENGLANDeng
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