Impact of Cigarette Smoke Exposure on the Lung Fibroblastic Response after Influenza Pneumonia
| Autor: | Jung Yeon Lee, Virginia Brady, Chang Min Yoon, Charles S. Dela Cruz, Lokesh Sharma, Sreelakshmi Chandrasekharan, Nathaniel Andrews, Young Ae Kang, Santos Bermejo, Sei Won Lee, Wei Liu, Ashley Losier, Sang-Hun Kim, Min-Jong Kang |
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| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Pulmonary and Respiratory Medicine Pulmonary Fibrosis Pneumonia Viral Clinical Biochemistry Lung injury Virus Cigarette Smoking Mice 03 medical and health sciences 0302 clinical medicine Orthomyxoviridae Infections Fibrosis Influenza Human Humans Animals Medicine Fibroblast Lung Molecular Biology Cells Cultured Original Research Smokers business.industry Smoking Pneumonia Cell Biology Fibroblasts medicine.disease Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure 030228 respiratory system Influenza A virus Immunology business Ex vivo Transforming growth factor |
| Zdroj: | American Journal of Respiratory Cell and Molecular Biology. 59:770-781 |
| ISSN: | 1535-4989 1044-1549 |
| DOI: | 10.1165/rcmb.2018-0004oc |
| Popis: | Influenza viruses can result in significant lung injury with significant morbidity and mortality. In this study, we evaluated the impact of cigarette smoke (CS) exposure on the pulmonary fibroblastic response after influenza infection. We used a murine model in which animals were exposed to CS or room air and subsequently infected with H1N1 influenza virus. Inflammatory and fibrotic responses were measured at different time points after influenza infection. Primary fibroblasts were isolated from the lungs of mice and their characteristics were evaluated. Exposure to CS significantly increased the amount of collagen in the lungs of mice infected with influenza virus compared with the nonsmoking group at 30 days after infection. Furthermore, the presence of fibroblast-specific protein–positive cells increased in the lungs of influenza-infected mice that were exposed to CS compared with the infection-alone group. The smoking group also showed delays in weight recovery and higher cell counts in BAL fluid after infection. Active transforming growth factor β1 levels in BAL fluid increased in both groups; however, CS-exposed mice had a later surge in active transforming growth factor β1 (Day 24). Ex vivo cultures of lung-derived fibroblasts from CS-exposed mice with influenza infection showed rapid proliferation, increased expression of α-smooth muscle actin–stained stress fibers, and higher expression of growth factors compared with fibroblasts from room air–exposed lungs after infection. These results suggest that CS exposure changes the fibroblastic potential, leading to increased fibrosis after influenza infection. |
| Databáze: | OpenAIRE |
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