Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA224759 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Type I IFN-signaling suppresses an excessive IFN-{gamma} response and prevents lung damage and chronic inflammation following Pneumocystis (PC)-infection and clearance in CD4 T cell-competent mice. Type I IFN -signaling in pulmonary CD11c+ DCs and alveolar macrophages may prevent chronic inflammation following PC lung infection and clearance by suppressing an excessive IFN-g-response via the induction of SOCS1. IFNAR-/- and wildtype mice were both Pneumocystis infected via itratracheal instillation. Pulmonary CD11c+ cells were isolated from collagen digested lungs at day 7 and day 14 post infection from both wildtype and IFNAR-/- mice using a magnetic cell sorting technique from Miltenyi with CD11c microbeads. Cells from three individual animals per group were isolated and assessed. Comparison of 2 treatment types at 2 timepoints to determine whether type I IFN signaling is initiated in resident and early recruited pulmonary CD11c+ cells following Pneumocystis lung infection and whether this is relevant to the outcome of the inflammatory response during the initiation of clearance.
2010-07-07 | E-GEOD-18607 | biostudies-arrayexpress
Project description:Pulmonary hypertension (PH) is a disease of diverse etiology. While primary PH can develop in the absence of prior disease, PH more commonly develops in conjunction with other pulmonary pathologies. We previously reported a mouse model in which PH occurs as a sequelae of Pneumocystis infection in the context of transient CD4 depletion. Here, we demonstrate that instead of the expected Th2 pathways, the Th1 cytokine IFN-M-NM-3 was essential for the development of PH, as wild type mice developed PH, but not IFN-M-NM-3 knockout mice. Because gene expression analysis showed few strain differences that were not immune function related, we focused on those responses as potential pathologic mechanisms. While there were several differences in cellular and cytokine response that warrant further examination, we focused on three important aspects. First, if CD4 cells were continuously depleted, but the infection was limited by antibiotic treatment, then PH did not occur, confirming that CD4 T-cells are required for PH development. Second, although CD8 T-cells are implicated in the pathology of unabated Pneumocystis pneumonia, they did not have a role in the onset of PH. Finally, although there are differences in the amounts of the pulmonary immune cells, differences existed in phenotypes of immune cells that correlated with PH, such as elevated CD204 expression in lung CD11c+ cells. Two groups of BALB/c mice (3 per group) were infected i.t. with 10e7 Pneumocystis; one of those groups also received 4 injections of CD4 T-cell depleting antibodies beginning 3 days prior to infection and ending 7 days after infection. A third group was IFN-gamma knockout mice infected with Pneumocystis and depleted of CD4 cells in the same way. A fourth group of control non-treated BALB/c mice were also used. AT 38 days post infection, lung tissues were taken, and RNA was extracted to allow for differential gene expression analysis
2013-10-27 | E-GEOD-51750 | biostudies-arrayexpress
Project description:Type I IFN-signaling suppresses an excessive IFN-{gamma} response and prevents lung damage and chronic inflammation following Pneumocystis (PC)-infection and clearance in CD4 T cell-competent mice. Type I IFN -signaling in pulmonary CD11c+ DCs and alveolar macrophages may prevent chronic inflammation following PC lung infection and clearance by suppressing an excessive IFN-g-response via the induction of SOCS1.
2010-07-07 | GSE18607 | GEO
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.
2021-11-25 | GSE189407 | GEO
Project description:To evaluate the differential impact of IFN-gamma secretion on nasal cavity epithelial cells, we compared the transcriptional profiles of nasal cavity epithelial cells (CD45-, CD3- CD11b-, CD31-, CD326+) from wildtype and IFN-gamma knockout mice at 30 days (d30) post intranasal infection with a live attenuated influenza virus expressing the immunodominant H-2Kd CD8 T cell epitope from Sendai virus nucleoprotein (LAIV-SenNP). Nasal cavity epithelial cells were also analyzed from LAIV-SenNP immunized wildtype and IFN-gamma knockout mice 3 days after intranasal administration of Sendai virus nucleoprotein peptide (d30+3). The results indicate that nasal cavity epithelial cells express genes associated with antigen presentation and antiviral function following antigen-specific T cell activation, and these alterations in transcriptional programming depend on IFN-gamma secretion.
2024-02-15 | GSE247376 | GEO
Project description:T cell response exert critical roles in the host adaptive immunity against Pneumocystis. However, the dynamics and diversity of T cell immune repertoire in HIV-negative Pneumocystis remains unknown. In this study, single-cell RNA and T cell receptor (TCR) sequencing were applied on cells sorted from lung tissues of mice infected with Pneumocystis from 0 to 4 weeks. Our data demonstrated clonally CD4+ T cells and CD8+ T cells expanded in response to Pneumocystis, which marked by highly expressed genes associated with T cell activation and cytotoxicity. The length distribution of CDR3 AA and gene usage variability were similar between Pneumocystis infected mice and control group. We tracked the transcriptome and TCR immune repertoires profiles of expanded lymphocyte clones during Pneumocystis infection, which demonstrate a reconstitution of the TCR immune repertoire after Pneumocystis infection.
2021-03-26 | GSE156843 | GEO
Project description:Mouse lung samples from mice challenged with OVA or PBS control. Wildtype (B6) mice were tested, as well as mast cell deficient mice with engraftment of normal mast cells and mast cells deficient in IgE or Ifn-gamma signaling. Treatment/Control
2014-02-02 | E-GEOD-27066 | biostudies-arrayexpress
Project description:Mouse lung samples from mice challenged with OVA or PBS control. Wildtype (B6) mice were tested, as well as mast cell deficient mice with engraftment of normal mast cells and mast cells deficient in IgE or Ifn-gamma signaling.
2014-02-02 | GSE27066 | GEO
Project description:Pulmonary hypertension (PH) is a disease of diverse etiology. While primary PH can develop in the absence of prior disease, PH more commonly develops in conjunction with other pulmonary pathologies. We previously reported a mouse model in which PH occurs as a sequelae of Pneumocystis infection in the context of transient CD4 depletion. Here, we demonstrate that instead of the expected Th2 pathways, the Th1 cytokine IFN-γ was essential for the development of PH, as wild type mice developed PH, but not IFN-γ knockout mice. Because gene expression analysis showed few strain differences that were not immune function related, we focused on those responses as potential pathologic mechanisms. While there were several differences in cellular and cytokine response that warrant further examination, we focused on three important aspects. First, if CD4 cells were continuously depleted, but the infection was limited by antibiotic treatment, then PH did not occur, confirming that CD4 T-cells are required for PH development. Second, although CD8 T-cells are implicated in the pathology of unabated Pneumocystis pneumonia, they did not have a role in the onset of PH. Finally, although there are differences in the amounts of the pulmonary immune cells, differences existed in phenotypes of immune cells that correlated with PH, such as elevated CD204 expression in lung CD11c+ cells.
2013-10-27 | GSE51750 | GEO
Project description:To investigate the early host response triggered by three different strains of Trypanosoma cruzi at a local infection site, changes in host gene expression were monitored in a murine intradermal infection model using Affymetrix oligonucleotide arrays. Robust induction of IFN-stimulated genes (ISGs) was observed in excised skin 24 hours post-infection where the level of ISG induction was parasite strain-dependent with the least virulent strain triggering a muted IFN response. Infection of mice immunodepleted of IFNγ-producing cells or infection of IFNγ-deficient mice had minimal impact on the IFN response generated in T. cruzi infected mice. In contrast, infection of mice lacking the type I IFN receptor demonstrated that type I IFNs are largely responsible for the IFN response generated at the site of infection. These data highlight type I IFNs as important components of the innate immune response to T. cruzi the site of inoculation and their role in shaping the early transcriptional response to this pathogen. We used microarrays to detail the local host transcriptional response to intradermal T. cruzi infection in WT mice and mice depleted of NK cells, or deficient in IFN-gamma or type I IFN responses. Additionally we compared the local host-transcriptional response generated to infection with 3 different strains of Trypanosoma cruzi (Y, Brazil, and G). Experiment Overall Design: Mice were infected by intradermal injection of 10^6 T. cruzi trypomastigotes in 100uL of saline split between 2 adjacent sites on the shaved side flank. Control mice were injected with an equal volume of saline. 24 hours post-injection approximately 75mm^2 of skin immediately surrounding the injection site was excised and RNA was isolated from the tissue. Balb/c mice were used for most experiments and IFN-gamma KO mice were on the Balb/c background. WT 129 mice were also used as IFNAR-/- mice were on the 129 background. In total 33 arrays were performed. 7 WT (Balb/c) control, 3 Y strain infected, 3 Brazil strain infected, 3 G strain infected, 2 IFN-gamma KO control, 2 IFN-gamma KO infected, 1 NK cell depleted control, 1 NK cell depleted infected, 3 WT (129) control, 3 WT (129) infected, 3 IFNAR KO control, 3 IFNAR KO infected
2009-01-14 | E-GEOD-13522 | biostudies-arrayexpress