The PSD4 gene, which is involved in membrane recycling [61], and CHMP5, which is an essential regulator of late endosome function. CHMP5 null cells show enhanced signal transduction, protein accumulation

in enlarged multi vesicular bodies (MVB) and inhibition of MVB trafficking to lysosomes [62]. In addition, we have recently found that markers of multi lamellar/multi vesicular bodies associate with membrane structures within the PV lumen during C. burnetii infection of Vero cells (unpublished observations). Given that C. burnetii’s LY2835219 replication niche possesses markers see more consistent with those on late endosomes/lysosomes [2], our finding that expression of these genes are markedly lower when C. burnetii protein synthesis is inhibited suggests that they play a part in development and maintenance of the PV during infection. This overall manipulation learn more of endocytosis, vesicle trafficking, and late endosome/lysosome maturation is in agreement with studies which found that inhibition of C.

burnetii protein synthesis at any point during the life cycle changes these processes within C. burnetii infected cells [35, 63]. Conclusions Through this study we have discovered thirty-six host cell genes with significant relative expression changes after transient inhibition of C. burnetii protein synthesis. The expression changes of these genes in the mock and CAM treatment conditions were confirmed using RT-qPCR analysis. Using bioinformatics, we have also determined the predominant host cell processes associated with these genes. Collectively, these data support our hypothesis that C. burnetii proteins differentially modulate host cell genes during infection. Predominant cellular functions

that are modulated by C. burnetii proteins include (i) innate immune response   (ii) cell death and proliferation   (iii) vesicle trafficking and development   (iv) lipid homeostasis, and   (v) cytoskeletal function   These findings indicate that C. burnetii actively modulates the expression of genes that may play a role in the ability of the pathogen to establish the PV, survive, and replicate within the intracellular environment. Acknowledgements We wish to thank Drs. Dan Stein, and Clint Krehbiel, and Mr. Rod Mills for technical advice MycoClean Mycoplasma Removal Kit and direction in performing microarrays. We would like to thank Dr. Kent Morgan for technical advice in RT-qPCR analysis. We also thank Dr. Rolf Prade for the critical reading of this manuscript. This research was supported by National Institutes of Health grant R15 A1072710 (E.I.S.). Electronic supplementary material Additional file 1: Tables S1.A-I. Excel file containing Tables S1.A through S1.I as individual tab-accessible tables within a single file (Supplemental Table S1.A-I). (XLSX 898 KB) Additional file 2: Figure S1.