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Título:	An investigation of the resolution of inflammation (catabasis) in COPD.
Autor/a:	Noguera, Aina; Gomez, Cristina; Faner, Rosa; Cosío, Borja G.; González Périz, Ana; Clària i Enrich, Joan; Carvajal, Angel; Agustí García-Navarro, Àlvar
Notas:	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.
Materia(s):	-Malalties pulmonars obstructives cròniques -Bronquitis -Immunologia -Chronic obstructive pulmonary diseases -Bronchitis -Immunology
Derechos:	cc-by (c) Noguera, A. et al., 2012 http://creativecommons.org/licenses/by/3.0/es
Tipo de documento:	Artículo Artículo - Versión publicada
Editor:	BioMed Central
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