Project description:Comparison of kidney and liver samples from wildtype C3HeB/FeJ mice. 16 dual-color DNA-chip hybridizations of cDNAs from three age-matched male mice were made. For each individual mouse 6 or 4 replicate hybridizations were done. Keywords = liver Keywords = kidney Keywords = C3HeB/FeJ Keywords: other
Project description:In-vivo Gene Signatures of Mycobacterium tuberculosis In C3HeB/FeJ Mice In this experiment we have compared Mtb transcriptomics in-vivo, using samples derived from chronically infected C3HeB/FeJ mice, which produce human like caseating lesions, unlike other murine species, to Mtb cultured in-vitro. Similarly, the genome-wide expression of MtbdeldosR, MtbdeldosS and MtbdeldosT mutants is also compared between lungs from C3HeB/FeJ mice and in-vitro culturing.
Project description:Only a minority of M. tuberculosis-infected individuals progress to tuberculosis, however the early immune mechanisms determining outcome are unclear. C3HeB/FeJ mice display high, partially type I IFN-dependent, tuberculosis susceptibility, compared to relatively tuberculosis-resistant C57BL/6 mice. Using bulk and scRNA-seq over the first weeks of M. tuberculosis infection, we describe an unexpected, higher early pulmonary type I IFN response in C57BL/6 than C3HeB/FeJ mice, accompanying more pronounced early monocyte-derived macrophage (MDM) accumulation and lesion formation. The C57BL/6 type I IFN response plateaued with formation of extensive CD4+ T cell-MDM interactions in lesions, accompanied by high expression of T cell-attractant chemokines by MDMs. Conversely, delayed immune initiation in C3HeB/FeJ mice preceded rapid domination of lesions by inflammatory neutrophils, depletion of which enhanced CD4+ T cell-MDM interactions. Type I IFNs unexpectedly promoted early bacterial replication and limited lesion CD4+ T cell numbers in both C57BL/6 and C3HeB/FeJ mice, while pronounced later effects on inflammatory neutrophil activation were observed in C3HeB/FeJ, suggestive of context-dependent effects of type I IFNs during M. tuberculosis infection.
Project description:Only a minority of M. tuberculosis-infected individuals progress to tuberculosis, however the early immune mechanisms determining outcome are unclear. C3HeB/FeJ mice display high, partially type I IFN-dependent, tuberculosis susceptibility, compared to relatively tuberculosis-resistant C57BL/6 mice. Using bulk and scRNA-seq over the first weeks of M. tuberculosis infection, we describe an unexpected, higher early pulmonary type I IFN response in C57BL/6 than C3HeB/FeJ mice, accompanying more pronounced early monocyte-derived macrophage (MDM) accumulation and lesion formation. The C57BL/6 type I IFN response plateaued with formation of extensive CD4+ T cell-MDM interactions in lesions, accompanied by high expression of T cell-attractant chemokines by MDMs. Conversely, delayed immune initiation in C3HeB/FeJ mice preceded rapid domination of lesions by inflammatory neutrophils, depletion of which enhanced CD4+ T cell-MDM interactions. Type I IFNs unexpectedly promoted early bacterial replication and limited lesion CD4+ T cell numbers in both C57BL/6 and C3HeB/FeJ mice, while pronounced later effects on inflammatory neutrophil activation were observed in C3HeB/FeJ, suggestive of context-dependent effects of type I IFNs during M. tuberculosis infection.
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
