Project description:Bovine tuberculosis, caused by Mycobacterium bovis, is a disease of considerable economic importance yet comparatively little is known about the bovine immune response to the disease. Alveolar macrophages are one of the first cells to encounter mycobacteria following infection. In this experiment we investigated the early transcriptional response of bovine alveolar macrophages following infection with M. bovis. The transcriptional response to heat-killed M. bovis was also investigated to look for genes that are only differentially transcribed in response to the live organism. Five-condition experiment, uninfected, live and heat-killed M. bovis-infected bovine alveolar macrophages from five cattle infected for two and four hours. Comparisons were within animal. Dye swaps were incorporated into the design.
Project description:Bovine tuberculosis, caused by Mycobacterium bovis, is a disease of considerable economic importance yet comparatively little is known about the bovine immune response to the disease. Alveolar macrophages are one of the first cells to encounter mycobacteria following infection. In this experiment we investigated the early transcriptional response of bovine alveolar macrophages following infection with M. bovis. The transcriptional response to heat-killed M. bovis was also investigated to look for genes that are only differentially transcribed in response to the live organism.
Project description:Transcriptional profiling of splenic lymphocytes derived from vaccinated mice, and ex-vivo exposed to M.tb.-infected macrophages in culture. Splenocytes from mice innoculated with Mycobacterium bovis BCG Pasteur (PAS), or M. bovis BCG Copenhagen (SSI), or heat killed BCG SSI (HK), or uninfected control, were ex vivo co-cultured with mouse bone marrow macrophages previously infected with M. tb.
Project description:The aim of this study was to identify the signaling pathways differentially engaged upon infection with either live or heat killed Mycobacterium tuberculosis in murine bone marrow derived macrophages. Based on preliminary data that type I IFN signaling dominates the transcriptional differences, we investigated what roles the type I IFN receptor IFNAR and the signaling molecule STING play during infection with either live or heat killed Mycobacterium tuberculosis in bone marrow derived macrophages. In WT and STING KO macrophages, IFNbeta treatment was added either by itself or in addition to both of the infection conditions to test whether the lack of IFNbeta induction in these cells accounted for any differences in transcriptional respones.added IFNbeta treatment either by itself or in addition to both of the infection conditions.
Project description:Mycobacterium bovis (M. bovis) and Mycobacterium avium subspecies paratuberculosis (MAP) are important pathogens of cattle, causing bovine tuberculosis and Johne’s disease respectively. M. bovis and MAP infect residential macrophages in the lung and intestines respectively and subvert the macrophage biology to create a survival niche. To investigate this interaction we simultaneously studied the transcriptional response of bovine monocyte-derived macrophages to infection with two strains of M. bovis (AF2122/97 and G18) and two strains of MAP (C & L1).
Project description:Our goal is to discriminate specific genes in live M.leprae-infected peritoneal macrophages in comparison to heat-killed M.leprae infected peritoneal macrophages using microarray. Two-condition experiment, Heat-killed M.leprae infected macrophage vs. Live M.leprae infected macrophage. Biological replicates: 16 mice (control), 8 heat-killed M. leprae mice (sample 1), and 8 live M. leprae infected mice (sample 2). Independently grown and harvested from isolator. One replicate per array.
Project description:Mycobacterium bovis, the agent of bovine tuberculosis, causes an estimated $3 billion annual losses to global agriculture due, in part, to the limitations of current diagnostics. Development of next-generation diagnostics requires a greater understanding of the interaction between the pathogen and the bovine host. Therefore, to explore the early response of the alveolar macrophage to infection, we report the first application of RNA-sequencing to define, in exquisite detail, the transcriptomes of M. bovis-infected and non-infected alveolar macrophages from ten calves at 2, 6, 24 and 48 hours post-infection. Differentially expressed sense genes were detected at these time points that revealed enrichment of innate immune signalling functions, and transcriptional suppression of host defence mechanisms (e.g., lysosome maturation). We also detected differentially expressed natural antisense transcripts, which may play a role in subverting innate immune mechanisms following infection. Furthermore, we report differential expression of novel bovine genes, some of which have immune-related functions based on orthology with human proteins. This is the first in-depth transcriptomics investigation of the alveolar macrophage response to the early stages of M. bovis infection and reveals complex patterns of gene expression and regulation that underlie the immunomodulatory mechanisms used by M. bovis to evade host defence mechanisms.
