Identifier to cite or link to this item: http://hdl.handle.net/20.500.13003/12976
An investigation of the resolution of inflammation (catabasis) in COPD
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CitationNoguera A, Gomez C, Faner R, Cosio B, Gonzalez-Periz A, Claria J, et al. An investigation of the resolution of inflammation (catabasis) in COPD. Respir Res. 2012 Nov 13;13:101.
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 TGF beta, 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 TGF beta in lung macrophages; (2) real time PCR to determine HGF, PPAR gamma, TGF beta, 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 TGF beta, VEGF, HGF, PPAR gamma, 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.
Pulmonary Disease, Chronic Obstructive
Enfermedad Pulmonar Obstructiva Crónica
Persona de Mediana Edad