Modelling COPD in Drosophila Melanogaster by cigarette smoke inhalation exposure: Alterations in the expression of COPD-relevant orthologous genes

<bold>Introduction:</bold> Cigarette smoking is the main risk factor for chronic obstructive pulmonary disease (COPD), thus relevant animal models are critical. <bold>Aims:</bold> Based on <italic>in silico</italic> predicted COPD-relevant orthologous genes between humans and <italic>Drosophila melanogaster</italic> in this study, we used the same model organism to assess the effect of cigarette smoke (CS) inhalation on the expression pattern of specific candidate genes for COPD. <bold>Methods:</bold> Adult wild type flies were exposed to CS via inhalation, 15 minutes per day for 5 days. Primers specific for the Drosophila <italic>FUCT6, Prosapl, Raptor, CG1134, Pdss2, CG4562, CG8460, Ddx1, Pli, AP-2alpha, CG31751, Msh6, Liprin-Gamma, Ced-12</italic> transcripts were designed, and qRT-PCR was performed with ribosomal protein <italic>L32</italic> as the gene of reference. Fold changes were assessed with the 2^–∆∆Ct method. Experiments were repeated thrice. <bold>Results:</bold> Four (<italic>FUCT6, Pdss2, Ddx1, Ced-12</italic>) and nine (<italic>FUCT6, CG1134, CG4562, Ddx1, AP-2alpha, CG31751, Msh6, Liprin-Gamma, Ced-12</italic>) genes were differentially expressed in CS-exposed male and female flies as compared to controls respectively. The human orthologs of these genes have been reported as key COPD-related genes in GWAS studies. <bold>Conclusions:</bold> CS inhalation exposure of adult fruit flies induces COPD-related transcriptomic changes. These findings indicate that the fruit fly is a promising <italic>in vivo</italic> model to study CS-induced COPD.