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Article: Neutrophil-mediated degradation of lung proteoglycans: Stimulation by tumor necrosis factor-α in sputum of patients with bronchiectasis

TitleNeutrophil-mediated degradation of lung proteoglycans: Stimulation by tumor necrosis factor-α in sputum of patients with bronchiectasis
Authors
Issue Date2000
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
American Journal of Respiratory and Critical Care Medicine, 2000, v. 162 n. 5, p. 1925-1931 How to Cite?
AbstractNeutrophil-mediated degradation of bronchial matrix has been proposed as a pathogenetic factor in bronchiectasis. We hypothe-size that neutrophils, found in abundance in the bronchial lumens of patients with bronchiectasis, are capable of degrading lung matrix proteoglycans and that proinflammatory mediators in bronchial secretions of these patients can enhance the degradative action of neutrophils. We used rat bronchoalveolar proteoglycans entrapped in polyacrylamide gel beads as a substrate for test incubations with neutrophils from healthy volunteers and sputum sol from patients with idiopathic bronchiectasis. Coincubations with specimens of sputum sol and neutrophils showed proteoglycan degradation indices (PDIs) in excess of the sum of indices due to incubation with either heat-inactivated sputum sol or heat-inactivated neutrophils, suggesting sputum stimulation of the neutrophil response. Mediation of this stimulation by tumor necrosis factor (TNF)-α was suggested because (1) indices for the coincubations correlated with sputum levels of TNF-α and (2) an anti-TNF-α antibody completely attenuated the sputum-stimulated effect. Furthermore, recombinant human TNF-α required accompanying sputum sol to exert an enhancing effect on neutrophil-mediated proteoglycan degradation. Because neutrophil-mediated proteoglycan degradation in the coincubations was inhibited largely (90%) by Eglin C and much less so (8% to 20%) by ethylenediamine tetraacetic acid, we conclude that serine proteases secreted by neutrophils were mainly responsible for degradation of proteoglycans in the model matrix and that the secretion was stimulated by TNF-α in the presence of cofactors in the bronchial secretions of patients with bronchiectasis.
Persistent Identifierhttp://hdl.handle.net/10722/147444
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShum, DKYen_HK
dc.contributor.authorChan, SCHen_HK
dc.contributor.authorIp, MSMen_HK
dc.date.accessioned2012-05-29T06:03:45Z-
dc.date.available2012-05-29T06:03:45Z-
dc.date.issued2000en_HK
dc.identifier.citationAmerican Journal of Respiratory and Critical Care Medicine, 2000, v. 162 n. 5, p. 1925-1931en_HK
dc.identifier.issn1073-449Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/147444-
dc.description.abstractNeutrophil-mediated degradation of bronchial matrix has been proposed as a pathogenetic factor in bronchiectasis. We hypothe-size that neutrophils, found in abundance in the bronchial lumens of patients with bronchiectasis, are capable of degrading lung matrix proteoglycans and that proinflammatory mediators in bronchial secretions of these patients can enhance the degradative action of neutrophils. We used rat bronchoalveolar proteoglycans entrapped in polyacrylamide gel beads as a substrate for test incubations with neutrophils from healthy volunteers and sputum sol from patients with idiopathic bronchiectasis. Coincubations with specimens of sputum sol and neutrophils showed proteoglycan degradation indices (PDIs) in excess of the sum of indices due to incubation with either heat-inactivated sputum sol or heat-inactivated neutrophils, suggesting sputum stimulation of the neutrophil response. Mediation of this stimulation by tumor necrosis factor (TNF)-α was suggested because (1) indices for the coincubations correlated with sputum levels of TNF-α and (2) an anti-TNF-α antibody completely attenuated the sputum-stimulated effect. Furthermore, recombinant human TNF-α required accompanying sputum sol to exert an enhancing effect on neutrophil-mediated proteoglycan degradation. Because neutrophil-mediated proteoglycan degradation in the coincubations was inhibited largely (90%) by Eglin C and much less so (8% to 20%) by ethylenediamine tetraacetic acid, we conclude that serine proteases secreted by neutrophils were mainly responsible for degradation of proteoglycans in the model matrix and that the secretion was stimulated by TNF-α in the presence of cofactors in the bronchial secretions of patients with bronchiectasis.en_HK
dc.languageengen_US
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.orgen_HK
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicineen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshBronchiectasis - Metabolismen_US
dc.subject.meshBronchoalveolar Lavage Fluid - Chemistryen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLung - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshNeutrophils - Physiologyen_US
dc.subject.meshProteoglycans - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSputum - Chemistryen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Analysis - Pharmacologyen_US
dc.titleNeutrophil-mediated degradation of lung proteoglycans: Stimulation by tumor necrosis factor-α in sputum of patients with bronchiectasisen_HK
dc.typeArticleen_HK
dc.identifier.emailShum, DKY:shumdkhk@hkucc.hku.hken_HK
dc.identifier.emailIp, MSM:msmip@hku.hken_HK
dc.identifier.authorityShum, DKY=rp00321en_HK
dc.identifier.authorityIp, MSM=rp00347en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid11069836-
dc.identifier.scopuseid_2-s2.0-0033679026en_HK
dc.identifier.hkuros61136-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033679026&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume162en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1925en_HK
dc.identifier.epage1931en_HK
dc.identifier.isiWOS:000165202900056-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShum, DKY=7004824447en_HK
dc.identifier.scopusauthoridChan, SCH=35261745200en_HK
dc.identifier.scopusauthoridIp, MSM=7102423259en_HK

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