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MicroRNA-155 Deficiency Protects Mice from Smoke-Induced Inflammation
Description
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A7426 - MicroRNA-155 Deficiency Protects Mice from Smoke-Induced Inflammation
Author Block: E. G. De Smet1, P. Mestdagh2, F. Avila Cobos2, E. Blomme1, S. Provoost1, T. Maes1, G. F. Joos1, G. G. Brusselle1, K. R. Bracke1; 1Respiratory Medicine, Ghent University Hospital, Ghent, Belgium, 2Center for Medical Genetics, Ghent University, Ghent, Belgium.
RATIONALE
MicroRNAs (miRNAs) are short, non-coding single stranded RNA molecules that are involved in the regulation of gene expression. Studies using miR-155 deficient animals have established a role for miR-155 in the inflammatory response. We have previously demonstrated increased expression of miR-155 in lung tissue of smokers and patients with COPD compared to never smokers and in lung tissue of mice exposed to cigarette smoke compared to air-exposed mice. The aim of this study was to examine the function of miR-155 in a model of smoke-induced inflammation.
METHODS
B6.Cg-Mir155tm1.1Rsky/J (miR-155 KO) mice and C57BL/6J (Wild Type, WT) mice were exposed to cigarette smoke or air during 4 weeks. After this period, the mice were sacrificed and the inflammatory profile in broncho-alveolar lavage (BAL) fluid and lungs was analysed by flow cytometry.
RESULTS
Cigarette smoke exposure in WT mice resulted in an increase in the number and percentage of neutrophils, dendritic cells (DCs), innate lymphoid cells (ILCs) and T lymphocytes (CD4+ and CD8+) in BAL fluid. In miR-155 KO mice the cigarette smoke-induced increase of these cell types is attenuated (neutrophils, DCs, CD4+ T lymphocytes) or even absent (ILCs). Intracellular cytokine staining (IFN-γ, IL-13 and IL-17) revealed that all T helper subsets (Th1, Th2 and Th17) were increased after CS exposure in WT mice and that this increase was attenuated in the miR-155 KO mice. In lung tissue we observed an increase in the numbers and percentages of DCs and T lymphocytes (CD4+ and CD8+) after CS-exposure in WT and miR-155 KO mice. Similar to the results in BAL fluid, the increase in DCs and CD4+ T lymphocytes in the lung was attenuated in miR-155 KO mice compared to WT mice. In addition, activation of T lymphocytes (as measured by CD69 expression) was reduced in lung tissue of miR-155 KO mice compared to WT mice.
CONCLUSION
These results demonstrate that miR-155 is involved in the inflammatory response observed in cigarette-smoke induced inflammation.
Author Block: E. G. De Smet1, P. Mestdagh2, F. Avila Cobos2, E. Blomme1, S. Provoost1, T. Maes1, G. F. Joos1, G. G. Brusselle1, K. R. Bracke1; 1Respiratory Medicine, Ghent University Hospital, Ghent, Belgium, 2Center for Medical Genetics, Ghent University, Ghent, Belgium.
RATIONALE
MicroRNAs (miRNAs) are short, non-coding single stranded RNA molecules that are involved in the regulation of gene expression. Studies using miR-155 deficient animals have established a role for miR-155 in the inflammatory response. We have previously demonstrated increased expression of miR-155 in lung tissue of smokers and patients with COPD compared to never smokers and in lung tissue of mice exposed to cigarette smoke compared to air-exposed mice. The aim of this study was to examine the function of miR-155 in a model of smoke-induced inflammation.
METHODS
B6.Cg-Mir155tm1.1Rsky/J (miR-155 KO) mice and C57BL/6J (Wild Type, WT) mice were exposed to cigarette smoke or air during 4 weeks. After this period, the mice were sacrificed and the inflammatory profile in broncho-alveolar lavage (BAL) fluid and lungs was analysed by flow cytometry.
RESULTS
Cigarette smoke exposure in WT mice resulted in an increase in the number and percentage of neutrophils, dendritic cells (DCs), innate lymphoid cells (ILCs) and T lymphocytes (CD4+ and CD8+) in BAL fluid. In miR-155 KO mice the cigarette smoke-induced increase of these cell types is attenuated (neutrophils, DCs, CD4+ T lymphocytes) or even absent (ILCs). Intracellular cytokine staining (IFN-γ, IL-13 and IL-17) revealed that all T helper subsets (Th1, Th2 and Th17) were increased after CS exposure in WT mice and that this increase was attenuated in the miR-155 KO mice. In lung tissue we observed an increase in the numbers and percentages of DCs and T lymphocytes (CD4+ and CD8+) after CS-exposure in WT and miR-155 KO mice. Similar to the results in BAL fluid, the increase in DCs and CD4+ T lymphocytes in the lung was attenuated in miR-155 KO mice compared to WT mice. In addition, activation of T lymphocytes (as measured by CD69 expression) was reduced in lung tissue of miR-155 KO mice compared to WT mice.
CONCLUSION
These results demonstrate that miR-155 is involved in the inflammatory response observed in cigarette-smoke induced inflammation.
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