Il-17A contributes to maintenance of pulmonary homeostasis in a murine model of cigarette smoke-induced emphysema
| Autor: | Christoph Beisswenger, Bodo Wonnenberg, Michael D. Menger, Christian Herr, Andreas Kamyschnikow, M Voss, Philipp M. Lepper, Robert Bals, Michael Wegmann, Lisa Wolf, Anja Honecker |
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| Rok vydání: | 2015 |
| Předmět: |
Pulmonary and Respiratory Medicine
Physiology Pulmonary disease Respiratory Mucosa Real-Time Polymerase Chain Reaction Pulmonary function testing Mice Forced Expiratory Volume Physiology (medical) medicine Animals Homeostasis Cigarette smoke RNA Messenger Risk factor Cells Cultured Mice Knockout COPD Reverse Transcriptase Polymerase Chain Reaction business.industry Interleukin-17 Smoking Pneumonia Cell Biology medicine.disease Respiratory Function Tests Mice Inbred C57BL Pulmonary Alveoli Disease Models Animal Pulmonary Emphysema Murine model Immunology Cytokines Female business Bronchoalveolar Lavage Fluid |
| Zdroj: | American Journal of Physiology-Lung Cellular and Molecular Physiology. 309:L188-L195 |
| ISSN: | 1522-1504 1040-0605 |
| DOI: | 10.1152/ajplung.00388.2014 |
| Popis: | Smoking is the main risk factor for the development of the chronic obstructive pulmonary disease (COPD) in Western countries. Recent studies suggest that IL-17A and Th17 cells play a role in the pathogenesis of COPD. We used a murine model of chronic cigarette smoke (CS) exposure to explore the contribution of IL-17A to CS-induced lung damage and loss of pulmonary function. Histology and morphometry showed that IL-17A deficiency spontaneously resulted in a loss of lung structure under basal conditions. Even though inflammatory markers [IL-1β and granulocyte colony-stimulating factor (G-CSF)] were decreased in IL-17A-deficient mice (IL-17A−/−) exposed to CS compared with wild-type (WT) mice, IL-17A−/−mice were per se not protected from CS-induced emphysematous disease. Assessment of pulmonary function showed that IL-17A−/−mice were partially protected from CS-induced changes in total lung capacity. However, the respiratory elastance decreased and respiratory compliance increased in IL-17A−/−mice after exposure to CS. Morphometry revealed destruction of lung tissue in CS-exposed IL-17A−/−mice similar to WT mice. The expression of elastin was decreased in air-exposed IL-17A−/−mice and in CS-exposed WT and IL-17A−/−mice. Thus, in the present model of sterile CS-exposure, IL-17A contributes to normal lung homeostasis and does not mediate CS-induced loss of lung structure and pulmonary function. |
| Databáze: | OpenAIRE |
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