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- Publisher Website: 10.4049/jimmunol.167.8.4368
- Scopus: eid_2-s2.0-0035887772
- PMID: 11591761
- WOS: WOS:000171858300030
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Article: Protection from pulmonary fibrosis in the absence of CCR2 signaling
Title | Protection from pulmonary fibrosis in the absence of CCR2 signaling |
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Authors | |
Issue Date | 2001 |
Citation | Journal of Immunology, 2001, v. 167, n. 8, p. 4368-4377 How to Cite? |
Abstract | Pulmonary fibrosis can be modeled in animals by intratracheal instillation of FITC, which results in acute lung injury, inflammation, and extracellular matrix deposition. We have previously shown that despite chronic inflammation, this model of pulmonary fibrosis is lymphocyte independent. The CC chemokine monocyte-chemoattractant protein-1 is induced following FITC deposition. Therefore, we have investigated the contribution of the main monocyte-chemoattractant protein-1 chemokine receptor, CCR2, to the fibrotic disease process. We demonstrate that CCR2 -/- mice are protected from fibrosis in both the FITC and bleomycin pulmonary fibrosis models. The protection is specific for the absence of CCR2, as CCR5 -/- mice are not protected. The protection is not explained by differences in acute lung injury, or the magnitude or composition of inflammatory cells. FITC-treated CCR2 -/- mice display differential patterns of cellular activation as evidenced by the altered production of cytokines and growth factors following FITC inoculation compared with wild-type controls. CCR2 -/- mice have increased levels of GM-CSF and reduced levels of TNF-α compared with FITC-treated CCR2 +/+ mice. Thus, CCR2 signaling promotes a profibrotic cytokine cascade following FITC administration. |
Persistent Identifier | http://hdl.handle.net/10722/251596 |
ISSN | 2023 Impact Factor: 3.6 2023 SCImago Journal Rankings: 1.558 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Moore, B. B. | - |
dc.contributor.author | Paine, R. | - |
dc.contributor.author | Christensen, P. J. | - |
dc.contributor.author | Moore, T. A. | - |
dc.contributor.author | Sitterding, S. | - |
dc.contributor.author | Ngan, R. | - |
dc.contributor.author | Wilke, C. A. | - |
dc.contributor.author | Kuziel, W. A. | - |
dc.contributor.author | Toews, G. B. | - |
dc.date.accessioned | 2018-03-08T05:00:25Z | - |
dc.date.available | 2018-03-08T05:00:25Z | - |
dc.date.issued | 2001 | - |
dc.identifier.citation | Journal of Immunology, 2001, v. 167, n. 8, p. 4368-4377 | - |
dc.identifier.issn | 0022-1767 | - |
dc.identifier.uri | http://hdl.handle.net/10722/251596 | - |
dc.description.abstract | Pulmonary fibrosis can be modeled in animals by intratracheal instillation of FITC, which results in acute lung injury, inflammation, and extracellular matrix deposition. We have previously shown that despite chronic inflammation, this model of pulmonary fibrosis is lymphocyte independent. The CC chemokine monocyte-chemoattractant protein-1 is induced following FITC deposition. Therefore, we have investigated the contribution of the main monocyte-chemoattractant protein-1 chemokine receptor, CCR2, to the fibrotic disease process. We demonstrate that CCR2 -/- mice are protected from fibrosis in both the FITC and bleomycin pulmonary fibrosis models. The protection is specific for the absence of CCR2, as CCR5 -/- mice are not protected. The protection is not explained by differences in acute lung injury, or the magnitude or composition of inflammatory cells. FITC-treated CCR2 -/- mice display differential patterns of cellular activation as evidenced by the altered production of cytokines and growth factors following FITC inoculation compared with wild-type controls. CCR2 -/- mice have increased levels of GM-CSF and reduced levels of TNF-α compared with FITC-treated CCR2 +/+ mice. Thus, CCR2 signaling promotes a profibrotic cytokine cascade following FITC administration. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Immunology | - |
dc.title | Protection from pulmonary fibrosis in the absence of CCR2 signaling | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.4049/jimmunol.167.8.4368 | - |
dc.identifier.pmid | 11591761 | - |
dc.identifier.scopus | eid_2-s2.0-0035887772 | - |
dc.identifier.volume | 167 | - |
dc.identifier.issue | 8 | - |
dc.identifier.spage | 4368 | - |
dc.identifier.epage | 4377 | - |
dc.identifier.isi | WOS:000171858300030 | - |
dc.identifier.issnl | 0022-1767 | - |