Chronic LPS Inhalation Causes Emphysema-Like Changes in Mouse Lung that Are Associated with Apoptosis
| العنوان: | Chronic LPS Inhalation Causes Emphysema-Like Changes in Mouse Lung that Are Associated with Apoptosis |
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| المؤلفون: | Zhouwei Li, David A. Schwartz, John W. Hollingsworth, Eric Toloza, David M. Brass, William M. Foster, Erin N. Potts, Mark Cinque |
| المصدر: | American Journal of Respiratory Cell and Molecular Biology. 39:584-590 |
| بيانات النشر: | American Thoracic Society, 2008. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | Lipopolysaccharides, Male, Pulmonary and Respiratory Medicine, Pathology, medicine.medical_specialty, Time Factors, Lipopolysaccharide, Neutrophils, Clinical Biochemistry, Apoptosis, Caspase 3, Mice, chemistry.chemical_compound, Parenchyma, Animals, Medicine, Molecular Biology, Mice, Knockout, TUNEL assay, Lung, Inhalation, business.industry, Articles, Cell Biology, respiratory system, Procollagen peptidase, medicine.anatomical_structure, Gene Expression Regulation, Matrix Metalloproteinase 9, Pulmonary Emphysema, chemistry, Immunology, business, Procollagen |
| الوصف: | Lipopolysaccharide (LPS) is ubiquitous in the environment. Recent epidemiologic data suggest that occupational exposure to inhaled LPS can contribute to the progression of chronic obstructive pulmonary disease. To address the hypothesis that inhaled LPS can cause emphysema-like changes in mouse pulmonary parenchyma, we exposed C57BL/6 mice to aerosolized LPS daily for 4 weeks. By 3 days after the end of the 4-week exposure, LPS-exposed mice developed enlarged airspaces that persisted in the 4-week recovered mice. These architectural alterations in the lung are associated with enhanced type I, III, and IV procollagen mRNA as well as elevated levels of matrix metalloproteinase (MMP)-9 mRNA, all of which have been previously associated with human emphysema. Interestingly, MMP-9-deficient mice were not protected from the development of LPS-induced emphysema. However, we demonstrate that LPS-induced airspace enlargement was associated with apoptosis within the lung parenchyma, as shown by prominent TUNEL staining and elevated cleaved caspase 3 immunoreactivity. Antineutrophil antiserum-treated mice were partially protected from the lung destruction caused by chronic inhalation of LPS. Taken together, these findings demonstrate that inhaled LPS can cause neutrophil-dependent emphysematous changes in lung architecture that are associated with apoptosis and that these changes may be occurring through mechanisms different than those induced by cigarette smoke. |
| تدمد: | 1535-4989 1044-1549 |
| DOI: | 10.1165/rcmb.2007-0448oc |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4b1b826044e0c337ebb3236126255079 https://doi.org/10.1165/rcmb.2007-0448oc |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....4b1b826044e0c337ebb3236126255079 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15354989 10441549 |
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| DOI: | 10.1165/rcmb.2007-0448oc |