Project description:Macrophages were derived from the bone-marrow of 3 x fl/+ Dicer LysCre +/- (wild-type) and 3 x fl/fl Dicer LysCre +/- mice and stimulated with IL-4 (50ng/mL) for 72h. Total RNA was isolated and analyzed by gene array. In this experiment, we derived Dicer deficient bone-marrow macrophages using Dicer fl/+ LysM-Cre by Dicer fl/+ crossed mice to obtain Dicer fl/fl LysM-cre progeny (and Dicer deficient macrophages). Next, we studied the effects of IL-4 stimulation in macrophage with a deficiency in Dicer/microRNAs.
Project description:IL-6 induces IL4ralpha expression in macrophages. This mechanism is necessary to promote macrophage polarization towards an M2-phenotype and is crucial to limit the inflammatory response both upon obesity and LPS-endotoxemia. In this dataset, we include the expression data obtained from primary murine bone marrow-derived macrophages from control and IL6ralpha-deficient macrophages (n=4vs4) stimulated with interleukin-6 (IL-6) 8 samples were analyzed to compare control and IL6ralpha-deficient macrophages for their gene expression profiles upon stimulation with IL-6
Project description:We report the genome-wide RNA sequencing analysis in Il10-/- bone marrow-derived macrophages (BMDMs) stimulated by lipopolysaccharide (LPS) where IL-10 effect in macrophage inflammatory response was examined in IL-10-deficient BMDMs upon LPS stimulation with addition of exogenous IL-10.
Project description:Macrophages were derived from the bone-marrow of 3 x fl/+ Dicer LysCre +/- (wild-type) and 3 x fl/fl Dicer LysCre +/- mice and stimulated with IL-4 (50ng/mL) for 72h. Total RNA was isolated and analyzed by gene array.
Project description:We report the genomic regions enriched in Histone Deacetylase 3 (HDAC3) in mouse bone marrow derived macrophages. Furthermore, we also report the genomic acetylation pattern on Histone 3, Lysine 9 (H3K9) in macrophages with and without HDAC3 and/or treated with Th2 cytokine IL-4. HDAC3 enriched genomic regions in mouse bone marrow dervied macrophages and H3K9Ac enriched genomic regions in wild-type macrophages and macrophages treated with IL-4 and/or deficient in HDAC3.
Project description:Analysis of alternative activation of macrophages at gene expression level. The study forms part of a wider study where we compare the effects of IL-4 in different human and mouse macrophages. Our results support the notion that in vitro culture conditions greatly affect the macrophage response to IL-4. Total RNA obtained from bone marrow derived macrophages upon exposure to 20 ng/ml of IL-4 for 18 hours. Bone marrow derived macrophages were stimulated with the Th2 cytokine IL-4, for RNA extraction and hybridization on Affymetrix microarrays.
Project description:To analyse the Irf4-dependent transcriptional changes of mouse bone marrow-derived macrophages (BMM) in response to IL-4, we have employed whole genome microarray expression profiling. For this purpose, bone marrow cells were isolated from 8 to 12 weeks old Irf4-deficient or heterozygous mice and cultured in the presence of the macrophage colony-stimulating factor (M-CSF) . After seven days of culture, IL-4 was added for 4 and 18 hours. Keywords: Mouse strain comparision; Gene expression profiling IL-4 induced gene expression was investigated in mouse bone marrow-derived macrophages (BMM) of Irf4-deficient or heterozygous mice. BMM were incubated with mouse recombinant IL-4 for 4 or 18 hours or without for 18 hours. Three independent experiments were performed at each time point (mock, 4 and 18 hours) using littermates for each experiment.
Project description:Mitochondrial electron transport chain (ETC) function modulates macrophage biology, however, mechanisms underlying mitochondrial ETC control of macrophage immune responses are not fully understood. Here we report that mutant mice with mitochondrial ETC complex III (CIII)-deficient macrophages exhibit increased susceptibility to influenza A virus and LPS-induced endotoxic shock. Cultured bone marrow-derived macrophages (BMDMs) isolated from these mitochondrial CIII-deficient mice released less IL-10 than controls following TLR3 or TLR4 stimulation. Surprisingly, restoring mitochondrial respiration without generating superoxide using alternative oxidase (AOX) was not sufficient to reverse LPS-induced endotoxic shock susceptibility or restore IL-10 release. However, activation of protein kinase A (PKA) rescued IL-10 release in mitochondrial CIII-deficient BMDMs following LPS stimulation. Additionally, mitochondrial CIII deficiency did not affect BMDM responses to interleukin-4 (IL-4) stimulation. Thus, our results highlight the essential role of mitochondrial CIII generated superoxide in the release of anti-inflammatory IL-10 in response to TLR stimulation
