Chest
Clinical InvestigationsCOPDMatrix Metalloproteinases Activity in COPD Associated With Wood Smoke
Section snippets
Study Population
Twelve patients with COPD were examined. The diagnosis of COPD was confirmed by medical history and the results of pulmonary function tests. COPD was defined according to American Thoracic Society criteria.22 A history of productive daily cough for 3 consecutive months each year for the past 2 years, with an FEV1 of < 80% of the predicted value, an FEV1/FVC ratio of < 70%, and a reversibility in FEV1 of < 10% after inhalation of 400 μg salbutamol. Subjects with a history of asthma, atopy, or
Elastolytic Activity
Elastolytic activity using 3H-elastin-precoated wells was detected in all samples assayed (Fig 1). The mean WS and TS elastolytic activity (4.5 ± 1.27 and 3.0 ± 0.9 μg degraded elastin per 106 cells per 48 h, respectively) was significantly increased in comparison with the control group (1.42 ± 0.81 μg degraded elastin per 106 cells per 48 h; p < 0.05). Differences between WS and TS samples were not significant. Elastolytic activity was inhibited by EDTA but not by PMSF.
Gelatinolytic Activity
Zymography analysis
Discussion
The use of wood and other biomasses for cooking and heating is a very frequent practice worldwide, especially in developing countries, but respiratory alterations due to the exposure to WS scarcely have been investigated.192021 The clinical respiratory alterations associated with long-term WS exposure are the same as those for cigarette smoking. Moreover, chronic bronchitis and emphysema have been observed in non-tobacco smokers exposed to WS.29 The effects of TS on the inflammatory process and
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2015, Archivos de BronconeumologiaCitation Excerpt :The pro-inflammatory effects of biomass smoke are not restricted to the lung, since increases have been reported in CD8+ T-cells, natural killer (NK) cells, IL-6, IL-8, TNF-α, C-reactive protein (CRP) and monocyte chemoattractant protein (MCP)-1 in the blood of exposed individuals.67–69 Studies performed in samples of induced sputum, bronchoalveolar lavage (BAL) fluid and blood show that COPD patients exposed to biomass smoke have higher levels of inflammatory cells (neutrophils and eosinophils), IL-8, CRP and MMP-12, and increased MMP-9 activity, compared to control subjects.23,70,71 It has been suggested that biomass smoke may induce an inflammatory response via the Transient Potential Receptor (TRP) ion channels of the lung cells72 (Fig. 1).
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2015, Mucosal Immunology: Fourth EditionThe influence of 5-lipoxygenase on cigarette smoke-induced emphysema in mice
2014, Biochimica et Biophysica Acta - General SubjectsCitation Excerpt :Nonetheless, the increased expression of TIMP-1 in both the 5-LO−/− and CS 5-LO−/− control groups suggests a protective factor against the establishment of emphysema. It has been shown that other MMPs might contribute to emphysema [47–50], but it is likely that neutrophil elastase plays a significant role. In particular, it has been demonstrated that the lesion of the matrix, which results in emphysema, is the end-result of crosstalk between MMP-12 from macrophages and neutrophil elastase from neutrophils, with the latter protease more responsible for the greater portion of the final proteolytic attack [51,52].
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