Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA470835 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7145140.fastq.gz | Fastqsanger.gz | |||
| SRR7145141.fastq.gz | Fastqsanger.gz | |||
| SRR7145142.fastq.gz | Fastqsanger.gz | |||
| SRR7145143.fastq.gz | Fastqsanger.gz | |||
| SRR7145144.fastq.gz | Fastqsanger.gz |
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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: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:Pneumocystis is a pathogen of immunocompromised hosts but can also infect healthy hosts, in whom infection is rapidly controlled and cleared. To better understand the immune mechanisms contributing to clearance of infection, microarray methods were used to examine differential gene expression in the lungs of C57BL/6 and CD40 ligand knock-out (CD40L-KO) mice over time following exposure to Pneumocystis. Immuncompetent C57BL/6 mice, which control and clear infection efficiently, showed a robust response to infection characterized by the upregulation of 349 primarily immune-response associated genes. Temporal changes in the expression of these genes suggested that there was an early (week 2) primarily innate response, that waned without controlling infection; this were followed by primarily adaptive immune responses that peaked at week 5 and successfully cleared the infection. In conjunction with the latter, there was an increased expression of B cell associated (immunoglobulin) genes at week 6 that persisted through 11 weeks. In contrast, CD40L-KO mice, which are highly susceptible to developing severe Pneumocystis pneumonia, showed essentially no upregulation of immune-response associated genes at days 35 to 75. Immunohistochemical staining supported these observations by demonstrating an increase in CD4+, CD68+, and CD19+ cells in C57BL/6 but not CD40L-KO mice. Thus, the healthy host demonstrates a robust biphasic response to infection by Pneumocystis; CD40 ligand is an essential upstream regulator of the adaptive immune responses that efficiently control infection and prevent development of progressive pneumonia. Keywords: Time course response Pneumocystis murina infection wild type versus CD40L-KO mice
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Project description:Pneumocystis is a pathogen of immunocompromised hosts but can also infect healthy hosts, in whom infection is rapidly controlled and cleared. To better understand the immune mechanisms contributing to clearance of infection, microarray methods were used to examine differential gene expression in the lungs of C57BL/6 and CD40 ligand knock-out (CD40L-KO) mice over time following exposure to Pneumocystis. Immuncompetent C57BL/6 mice, which control and clear infection efficiently, showed a robust response to infection characterized by the upregulation of 349 primarily immune-response associated genes. Temporal changes in the expression of these genes suggested that there was an early (week 2) primarily innate response, that waned without controlling infection; this were followed by primarily adaptive immune responses that peaked at week 5 and successfully cleared the infection. In conjunction with the latter, there was an increased expression of B cell associated (immunoglobulin) genes at week 6 that persisted through 11 weeks. In contrast, CD40L-KO mice, which are highly susceptible to developing severe Pneumocystis pneumonia, showed essentially no upregulation of immune-response associated genes at days 35 to 75. Immunohistochemical staining supported these observations by demonstrating an increase in CD4+, CD68+, and CD19+ cells in C57BL/6 but not CD40L-KO mice. Thus, the healthy host demonstrates a robust biphasic response to infection by Pneumocystis; CD40 ligand is an essential upstream regulator of the adaptive immune responses that efficiently control infection and prevent development of progressive pneumonia. Keywords: Time course response Pneumocystis murina infection wild type versus CD40L-KO mice In experiment 1, C57BL/6 and CD40L-KO mice were co-housed in 2 cages; one cage was exposed to a P. murina-infected seeder, while the second was unexposed. Mice (3 per group) were sacrificed at day 32. Because the initial study demonstrated very little change in gene expression in CD40L-KO mice, only C57BL/6 mice were used for experiments 2 and 3. In Experiment 2, three cages (10 animals/cage) were set up: 2 cages were exposed to P. murina, and one was unexposed. Animals (5 per cage) were sacrificed at days 34 and 41. In Experiment 3, which focused on gene expression early after exposure to P. murina, five cages (9-10 animals/cage) were set up, of which 3 were exposed and 2 were unexposed. Animals (1-3 per cage) were sacrificed at days 7, 14 and 21 of exposure. Experiment 4 was designed to verify the initial results in CD40L-KO mice, and included 5 unexposed controls and 4 mice exposed for 35 days.
2008-12-22 | E-GEOD-11005 | biostudies-arrayexpress
Project description:B cells play vital roles in host defense against Pneumocystis infection, however, the features of B cell receptor (BCR) repertoire in the disease progression remain unclear. Here we integrated single-cell RNA sequencing and single-cell BCR sequencing of immune cells from mice lung at uninfected state and 1-4 weeks postinfection, in order to illustrate the dynamic nature of B cell responses during Pneumocystis infection. We identified continuously increased plasma cells and an elevated ratio of (IgA+ IgG) to (IgD+ IgM) after infection. Moreover, Pneumocystis infection was associated with an increase of a naïve B subset characterized by elevated expression of the transcription factor ATF3. The proportion of clonal expanded cells progressively increased, with the BCR diversity decreased. Biased usage of V(D)J genes was observed, and the usage frequency of IGHV9-3 was elevated. Overall, these results present a detailed atlas of B cell transcriptional changes and BCR repertoire features in the context of Pneumocystis infection.
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Project description:Diffuse midline gliomas (DMGs) are lethal brain tumors characterized by p53-inactivating mutations and oncohistone H3.3K27M mutations that rewire the cellular response to genotoxic stress. Using RCAS/tv-a retroviruses and Cre recombinase to inactivate p53 and induce native H3.3K27M mutations in a lineage- and spatially-directed manner, we generated primary mouse tumors that recapitulate human DMG. Disrupting ataxia-telangiectasia mutated kinase (ATM) enhanced the efficacy of radiation therapy in murine and patient-derived DMG models, increasing survival. Microscopy-based in situ sequencing was used to spatially resolve transcriptional profiles in >750,000 single cells with or without ATM disruption and radiation therapy, revealing altered immune-neoplastic and endothelial cell interactions after treatment. An allelic series of primary murine DMG models with different p53 mutations confirmed that transactivation-independent p53 activity is a key mediator of radiosensitivity after ATM disruption. Our findings contribute primary DMG mouse models with deep profiling and reveal the mechanisms of treatment response to an actionable therapeutic strategy.
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Project description:Pneumocystis pneumonia (PCP) is an opportunistic infectious disease prevalent in immunosuppressive host. Corticosteroids treatment is the most significant risk factor for HIV-negative patients with PCP, though little is known about how corticosteroids alters the host defense against Pneumocystis infection. In the present study, we used transcriptomic analysis to examine the immune response in the lung of dexamethasone-treated PCP mice and compare the immune reaction of them with those without dexamethasone treatment.
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