Project description:Full title: Mouse Inflammatory Cytokines and Receptors Microarray-RNA profiling in lungs of WT, IFN-g-/- and IL-4-/- mice before and after Mycoplasma pulmonis infection RNA profiling of inflammatory chemokines, cytokines and receptors in lungs of 4-6 week old wild-type, IFN-g-/- and IL-4-/- BALB/cJ mice before and after 14-day Mycoplasma pulmonis infection
Project description:Full title: Mouse Inflammatory Cytokines and Receptors Microarray-RNA profiling in lungs of WT, IFN-g-/- and IL-4-/- mice before and after Mycoplasma pulmonis infection RNA profiling of inflammatory chemokines, cytokines and receptors in lungs of 4-6 week old wild-type, IFN-g-/- and IL-4-/- BALB/cJ mice before and after 14-day Mycoplasma pulmonis infection RNA pooled from lungs of each group- Uninfected and Infected; Experiment performed twice. With 3 mice in each of the uninfected and infected groups in the first experiment and 4 mice in each group in the second experiment; comparison Mycoplasma infected vs. uninfected mice within each strain of mice
Project description:RNA profiling of inflammatory chemokines, cytokines and receptors in AUTOMACS sorted F4/80+ and CD11c+ cells from lungs of 6-12 week old wild-type C3H/HeN mice before and after 14-day Mycoplasma pulmonis infection
Project description:RNA profiling of inflammatory chemokines, cytokines and receptors in AUTOMACS sorted F4/80+ and CD11c+ cells from lungs of 6-12 week old wild-type C3H/HeN mice before and after 14-day Mycoplasma pulmonis infection RNA pooled from pulmonary F4/80+ & CD11c+ cells of each group- Uninfected and Infected; Experiment performed twice. Comparison-RNA expression within each population of cells in Mycoplasma infected vs. uninfected mice
Project description:Mouse Inflammatory Cytokines and Receptors Microarray-RNA profiling in F4/80+ and CD11c+ cells from lungs of WT mice before and after Mycoplasma pulmonis infection
Project description:We sought to develop and characterize a novel paucibacillary model in mice, which develop necrotic lung granulomas following infection with Mycobacterium tuberculosis. Paucibacillary infection was established, recapitulating the sterilizing activities of human LTBI regimens. TNF neutralization led to increased lung bacillary load, disrupted granuloma architecture with expanded necrotic foci and reduced tissue hypoxia, and accelerated animal mortality. TNF-neutralized mouse lungs and sera showed significant upregulation of IFN?, IL-1?, IL-6, IL-10, CCL2, CCL3, and matrix metalloproteinase genes Six weeks after aerosol-immunization with recombinant M. bovis BCG overexpressing the 30-kilodalton antigen, C3HeB/FeJ mice were aerosol-infected with M. tuberculosis H37Rv. Six weeks later, mice were treated with one of three standard regimens for latent TB infection (LTBI) or TNF-neutralizing antibody. Mouse lungs were analyzed by histology, positron emission tomography/computed tomography, whole-genome microarrays, and RT-PCR. Lungs and sera were studied by multiplex enzyme-linked immunosorbent assays
Project description:Our previous data suggested that CXC ELR+ chemokines might be involved in neutrophil recruitment to the lungs during Coccidioides infection. To test that hypothesis, we infected IL-8R2 (Cxcr2) KO mice on a BALB/c background. IL-8R2 KO mice had fewer neutrophils in infected lungs than BALB/c controls, but unexpectedly the IL-8R2 KO mice also had 10-fold fewer organisms in their lungs than did control mice. To better understand the differences in IL-8R2 KO mouse lungs during Coccidioides infection we performed RNA-seq on lung tissue from uninfected and Coccidioides immitis infected mouse lungs in control and IL-8R2 (Cxcr2) KO mice. IL-8R2 KO mouse lungs had higher expression of genes associated with lymphocyte activation, including Th1 and Th17-related genes Ifnγ and Il17a and transcription factors Stat1 and Rorc. Bronchial alveolar lavage (BAL) fluid from infected IL-8R2 KO mice similarly contained more IL-17A and IFNγ.
Project description:RNA-Seq analysis of Treg cell subsets isolated from lungs of Il10GFPFoxp3Thy1.1 mice. Thy1.1+ Treg cells were FACS-sorted into IL-10–IL-18R–, IL-10+IL-18R– and IL10–IL-18R+ populations on day 5 following intranasal infection with 0.5 LD50 PR8-OTI influenza virus. mRNA profiles of each Thy1.1+ Treg cell population (IL-10–IL-18R–, IL-10+IL-18R– and IL10–IL-18R+) from lungs on day 5 following influenza infection from 5 infected mice, sorted into TRIzol LS reagent.
Project description:Influenza A Virus (IAV) triggers an exuberant host response that promotes acute lung injury. However, the determinants of the pathological host response to IAV remain incompletely understood. In the current study, we identified interferon (IFN)-γ-regulated subset of monocytes, CCR2+ monocytes, as a driver of lung damage during IAV pathogenesis. IFN-γ regulated the recruitment and inflammatory phenotype of CCR2+ monocytes, and CCR2 (CCR2-/-) and IFN-γ (IFN-γ-/-) deficient mice exhibited reduced lung inflammation, pathology, and increased resistance against bacterial co-infection by Streptococcus pneumoniae (Spn). Adoptive transfer of WT (IFN-γR1+), but not IFN-γR1 deficient (IFN-γR1-) CCR2+ monocytes, restored the wild-type (WT)-like pathological phenotype of lung damage in IAV-infected CCR2-/- mice. The CD8+ T cells were the most significant source of IFN-γ in IAV-infected lungs. Collectively, our data highlight that IFN-γ regulates CCR2+ monocyte-mediated lung pathology during IAV pathogenesis.
Project description:We used microarrays to analyse the global program of gene expression in response to Influenza A (X31) infection in lungs from C57BL/6 wt, 129S7 wt and IFNAR-/- (129) mice. Mock- or 5 day influenza A (X31)-infected total lungs from mice with the indicated genotypes were collected and processed for expression profiling.
