Project description:To this date, host transcriptome studies in leprosy have focused on Schwann cells, as well as mouse-footpad and skin biopsies. Despite macrophages being the most infected cell types in leprosy lesions, there is no genome-wide experiments with this model. Here, we aimed at identifying host macrophages transcriptional changes induced by live-Mycobacterium leprae infection for 48 hours.
Project description:Our object is to characterize the distinguish gene enrichment group in skin of Mycobacterium leprae (M. leprae)-infected footpads compared to that of Mycobacterium leprae (M. leprae) non-infected footpads.
Project description:Our object is to characterize the distinguish gene enrichment group in skin of Mycobacterium leprae (M. leprae)-infected footpads compared to that of Mycobacterium leprae (M. leprae) non-infected footpads. One-condition experiment, Skin of M. leprae non-infected footpads (control) vs. Skin of M. leprae infected footpads (sample). Biological replicates: 3 control and 3 sample, independently grown and harvested from isolator. One replicate per array.
Project description:Our goal is to understand the mechanism of granuloma formation in molecular level using Mycobacterium leprae (M. leprae)-infected footpads.
Project description:Our goal is to understand the mechanism of granuloma formation in molecular level using Mycobacterium leprae (M. leprae)-infected footpads. One-condition experiment, M. leprae non-infected footpads (control) vs. M. leprae infected footpads (sample). Biological replicates: 6 control, 6 (sample), independently grown and harvested from isolator. One replicate per array.
Project description:An opportunistic intracellular pathogen Mycobacterium intracellulare, a member of the nontuberculous mycobacteria (NTM) cluster, causes respiratory disease in immunosuppressed hosts, including companion dogs. The purpose of this study is to investigate a host-M.intracellulare interactome in canine monocyte-derived macrophages during the infection.
Project description:HIV-1 infection of monocyte-derived macrophages does not elicit a detectable type I IFN response in vitro, however, previously published data has shown that blocking STAT1 and STAT3 inhibits HIV-1 replication. Here we test to see if low levels of IFN inducible genes are detectable in human monocyte-derived macrophages that have been infected with HIV-1 in vitro.