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dc.contributor.author | Noguera, Aina |
---|---|
dc.contributor.author | Gomez, Cristina |
dc.contributor.author | Faner, Rosa |
dc.contributor.author | Cosío, Borja G. |
dc.contributor.author | González Périz, Ana |
dc.contributor.author | Clària i Enrich, Joan |
dc.contributor.author | Carvajal, Angel |
dc.contributor.author | Agustí García-Navarro, Àlvar |
dc.date | 2014-03-21T08:39:09Z |
dc.date | 2014-03-21T08:39:09Z |
dc.date | 2012-11-13 |
dc.date | 2014-03-21T08:39:09Z |
dc.identifier | 1465-9921 |
dc.identifier | 625715 |
dc.identifier | 23148928 |
dc.identifier.uri | http://hdl.handle.net/2445/52724 |
dc.description | Background: Chronic Obstructive Pulmonary Disease (COPD) is characterized by an enhanced inflammatory response to smoking that persists despite quitting. The resolution of inflammation (catabasis) is a complex and highly regulated process where tissue resident macrophages play a key role since they phagocytose apoptotic cells (efferocytosis), preventing their secondary necrosis and the spill-over of their pro-inflammatory cytoplasmic content, and release pro-resolution and tissue repair molecules, such as TGFβ, VEGF and HGF. Because inflammation does not resolve in COPD, we hypothesized that catabasis may be abnormal in these patients. Methods: To explore this hypothesis, we studied lung tissue samples obtained at surgery from 21 COPD patients,22 smokers with normal spirometry and 13 non-smokers controls. In these samples we used: (1)immunohistochemistry to assess the expression of CD44, CD36, VEGF and TGFβ in lung macrophages; (2) real time PCR to determine HGF, PPARγ, TGFβ, VEGF and MMP-9 gene expression; and, (3) ELISA to quantify lipoxin A4, a lipid mediator of catabasis. Results: We found that current and former smokers with COPD showed: (1) more inflammation (higher MMP-9 expression); (2) reduced macrophage surface expression of CD44, a key efferocytosis receptor; and, (3) similar levels of TGFβ, VEGF, HGF, PPARγ, and lipoxin A4 than smokers with normal spirometry, despite the presence of inflammation and disease. Conclusions: These results identify several potential abnormalities of catabasis in patients with COPD. |
dc.format | 9 p. |
dc.format | application/pdf |
dc.language | eng |
dc.publisher | BioMed Central |
dc.relation | Reproducció del document publicat a: http://dx.doi.org/10.1186/1465-9921-13-101 |
dc.relation | Respiratory Research, 2012, vol. 13, p. 101 |
dc.relation | http://dx.doi.org/10.1186/1465-9921-13-101 |
dc.rights | cc-by (c) Noguera, A. et al., 2012 |
dc.rights | http://creativecommons.org/licenses/by/3.0/es |
dc.rights | info:eu-repo/semantics/openAccess |
dc.subject | Malalties pulmonars obstructives cròniques |
dc.subject | Bronquitis |
dc.subject | Immunologia |
dc.subject | Chronic obstructive pulmonary diseases |
dc.subject | Bronchitis |
dc.subject | Immunology |
dc.title | An investigation of the resolution of inflammation (catabasis) in COPD. |
dc.type | info:eu-repo/semantics/article |
dc.type | info:eu-repo/semantics/publishedVersion |