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dc.contributor.author
Kolb, Martin
dc.contributor.author
Margetts, Peter J.
dc.contributor.author
Anthony, Daniel C.
dc.contributor.author
Pitossi, Fernando Juan
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dc.contributor.author
Gauldie, Jack
dc.date.available
2018-06-07T18:47:38Z
dc.date.issued
2001-06
dc.identifier.citation
Kolb, Martin; Margetts, Peter J.; Anthony, Daniel C.; Pitossi, Fernando Juan; Gauldie, Jack; Transient expression of IL-1β induces acute lung injury and chronic repair leading to pulmonary fibrosis; American Society for Clinical Investigation; Journal of Clinical Investigation; 107; 12; 6-2001; 1529-1536
dc.identifier.issn
0021-9738
dc.identifier.uri
http://hdl.handle.net/11336/47741
dc.description.abstract
IL-1beta is one of a family of proinflammatory cytokines thought to be involved in many acute and chronic diseases. Although it is considered to participate in wound repair, no major role has been attributed to IL-1beta in tissue fibrosis. We used adenoviral gene transfer to transiently overexpress IL-1beta in rat lungs after intratracheal administration. The high expression of IL-1beta in the first week after injection was accompanied by local increase of the proinflammatory cytokines IL-6 and TNF-alpha and a vigorous acute inflammatory tissue response with evidence of tissue injury. The profibrotic cytokines PDGF and TGF-beta1 were increased in lung fluid samples 1 week after peak expression of IL-1beta. Although PDGF returned to baseline in the third week, TGF-beta1 showed increased concentrations in bronchoalveolar lavage fluid for up to 60 days. This was associated with severe progressive tissue fibrosis in the lung, as shown by the presence of myofibroblasts, fibroblast foci, and significant extracellular accumulations of collagen and fibronectin. These data directly demonstrate how acute tissue injury in the lung, initiated by a highly proinflammatory cytokine, IL-1beta, converts to progressive fibrotic changes. IL-1beta should be considered a valid target for therapeutic intervention in diseases associated with fibrosis and tissue remodeling.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Society for Clinical Investigation
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Tgf-Â
dc.subject
Il-1
dc.subject.classification
Inmunología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Transient expression of IL-1β induces acute lung injury and chronic repair leading to pulmonary fibrosis
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-05-10T15:45:44Z
dc.identifier.eissn
1558-8238
dc.journal.volume
107
dc.journal.number
12
dc.journal.pagination
1529-1536
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Ann Arbor, Michigan
dc.description.fil
Fil: Kolb, Martin. McMaster University; Canadá
dc.description.fil
Fil: Margetts, Peter J.. McMaster University; Canadá
dc.description.fil
Fil: Anthony, Daniel C.. University of Southampton; Reino Unido
dc.description.fil
Fil: Pitossi, Fernando Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
dc.description.fil
Fil: Gauldie, Jack. McMaster University; Canadá
dc.journal.title
Journal of Clinical Investigation
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.jci.org/articles/view/12568
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1172/JCI12568
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