tetano
Editor, Senior Moderator
Am J Respir Cell Mol Biol. 2018 Aug 15. doi: 10.1165/rcmb.2018-0004OC. [Epub ahead of print]
[h=1]Impact of Cigarette Smoke Exposure on Lung Fibroblastic Response after Influenza Pneumonia.[/h] Lee SW[SUP]1[/SUP], Sharma L[SUP]2[/SUP], Kang YA[SUP]3[/SUP], Kim SH[SUP]4[/SUP], Chandrasekharan S[SUP]5[/SUP], Losier A[SUP]4[/SUP], Brady V[SUP]6[/SUP], Bermejo S[SUP]4[/SUP], Andrews N[SUP]7[/SUP], Yoon CM[SUP]4[/SUP], Liu W[SUP]7[/SUP], Lee JY[SUP]4[/SUP], Kang MJ[SUP]4[/SUP], Dela Cruz CS[SUP]8[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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 employed a murine model in which animals were exposed to cigarette smoke or room air and subsequently infected with H1N1 influenza virus. Inflammatory and fibrotic responses were measured at different time points post influenza infection. Primary fibroblasts were isolated from lung of mice and their characteristics were evaluated. Exposure to CS increased the amount of collagen in the lungs of mice infected with influenza virus and the amount was statistically significant at 30 days post infection, compared to the non-smoking group. Further, the presence of fibroblast specific protein positive cells increased in the lungs of influenza infected mice that were exposed to CS, compared to infection alone group. The smoking group also showed delay in weight recovery and higher cell counts in bronchoalveolar lavage (BAL) after infection. Active transforming growth factor (TGF)-β1 levels in the BAL fluid increased in both groups, however, smoke exposed mice had a later surge in active TGF-β1 (day 24). Ex vivo cultures of lung-derived fibroblasts from CS + influenza infection showed rapid proliferation, increased expression of α-smooth muscle actin stained stress fibers, and higher expression of growth factors compared with the fibroblasts from room air exposed lungs after infection. These results suggest that smoking exposure changes the fibroblastic potential leading to increased fibrosis after influenza infection.
[h=4]KEYWORDS:[/h] cigarette smoke; influenza virus; lung fibrosis; macrophages
PMID: 30110182 DOI: 10.1165/rcmb.2018-0004OC
[h=1]Impact of Cigarette Smoke Exposure on Lung Fibroblastic Response after Influenza Pneumonia.[/h] Lee SW[SUP]1[/SUP], Sharma L[SUP]2[/SUP], Kang YA[SUP]3[/SUP], Kim SH[SUP]4[/SUP], Chandrasekharan S[SUP]5[/SUP], Losier A[SUP]4[/SUP], Brady V[SUP]6[/SUP], Bermejo S[SUP]4[/SUP], Andrews N[SUP]7[/SUP], Yoon CM[SUP]4[/SUP], Liu W[SUP]7[/SUP], Lee JY[SUP]4[/SUP], Kang MJ[SUP]4[/SUP], Dela Cruz CS[SUP]8[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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 employed a murine model in which animals were exposed to cigarette smoke or room air and subsequently infected with H1N1 influenza virus. Inflammatory and fibrotic responses were measured at different time points post influenza infection. Primary fibroblasts were isolated from lung of mice and their characteristics were evaluated. Exposure to CS increased the amount of collagen in the lungs of mice infected with influenza virus and the amount was statistically significant at 30 days post infection, compared to the non-smoking group. Further, the presence of fibroblast specific protein positive cells increased in the lungs of influenza infected mice that were exposed to CS, compared to infection alone group. The smoking group also showed delay in weight recovery and higher cell counts in bronchoalveolar lavage (BAL) after infection. Active transforming growth factor (TGF)-β1 levels in the BAL fluid increased in both groups, however, smoke exposed mice had a later surge in active TGF-β1 (day 24). Ex vivo cultures of lung-derived fibroblasts from CS + influenza infection showed rapid proliferation, increased expression of α-smooth muscle actin stained stress fibers, and higher expression of growth factors compared with the fibroblasts from room air exposed lungs after infection. These results suggest that smoking exposure changes the fibroblastic potential leading to increased fibrosis after influenza infection.
[h=4]KEYWORDS:[/h] cigarette smoke; influenza virus; lung fibrosis; macrophages
PMID: 30110182 DOI: 10.1165/rcmb.2018-0004OC