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      Time course of cigarette smoke-induced pulmonary inflammation in mice.

      The European Respiratory Journal
      Animals, Bronchoalveolar Lavage Fluid, Cell Count, Dendritic Cells, Disease Models, Animal, Male, Mice, Mice, Inbred C57BL, Pneumonia, etiology, pathology, Pulmonary Emphysema, Smoking, adverse effects, Time Factors

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          Inflammation of the airways and lung parenchyma plays a major role in the pathogenesis of chronic obstructive pulmonary disease. In the present study a murine model of tobacco smoke-induced emphysema was used to investigate the time course of airway and pulmonary inflammatory response, with a special emphasis on pulmonary dendritic cell (DC) populations. Groups of mice were exposed to either cigarette smoke or to control air for up to 24 weeks. In response to cigarette smoke, inflammatory cells (i.e. neutrophils, macrophages and lymphocytes) progressively accumulated both in the airways and lung parenchyma of mice. Furthermore, a clear infiltration of DCs was observed in airways (10-fold increase) and lung parenchyma (1.5-fold increase) of cigarette-exposed mice at 24 weeks. Flow cytometric analysis of bronchoalveolar lavage (BAL) DCs of smoke-exposed mice showed upregulation of major histocompatability complex II molecules and costimulatory molecules CD40 and CD86, compared with BAL DCs of air-exposed mice. Morphometric analysis of lung histology demonstrated a significant increase in mean linear intercept and alveolar wall destruction after 24 weeks of smoke exposure. In conclusion, the time course of the changes in inflammatory and dendritic cells in both bronchoalveolar lavage and the pulmonary compartment of cigarette smoke-exposed mice was carefully characterised.

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          Animals,Bronchoalveolar Lavage Fluid,Cell Count,Dendritic Cells,Disease Models, Animal,Male,Mice,Mice, Inbred C57BL,Pneumonia,etiology,pathology,Pulmonary Emphysema,Smoking,adverse effects,Time Factors


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