Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA359930 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5139780_1.fastq.gz | Fastqsanger.gz | |||
| SRR5139780_2.fastq.gz | Fastqsanger.gz | |||
| SRR5139781_1.fastq.gz | Fastqsanger.gz | |||
| SRR5139781_2.fastq.gz | Fastqsanger.gz | |||
| SRR5139782_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 10 |
Similar Datasets
Project description:Examine differences in Type-1 alveolar epithelial cells with and without alveolar macrophages during influenza infection
2017-01-06 | GSE93085 | GEO
Project description:During influenza pneumonia, the alveolar epithelial cells of the lungs are targeted by influenza virus. The distal airway stem cells (DASCs) and proliferating alveolar type II (AT2) cells are reported to be putative lung repair cells. However, their relative spatial and temporal distribution is still unknown during influenza-induced acute lung injury. Here, we investigated the distribution of these cells, and concurrently performed global proteomic analysis of the infected lungs to elucidate and link the cellular and molecular events during influenza pneumonia recovery. BALB/c mice were infected with a sub-lethal dose of influenza H1N1 virus. From 5 to 25 days post-infection (dpi), mouse lungs were subjected to histopathologic and immunofluorescence analysis to probe for global distribution of lung repair cells (using P63 and KRT5 markers for DASCs; PCNA and SPC markers for AT2 cells). At 7 and 15 dpi, infected mouse lungs were also subjected to protein mass spectrometry for relative protein quantification. DASCs appeared only in the damaged area of the lung from 7 dpi onwards, reaching a peak at 21 dpi, and persisted at 25 dpi. However, no differentiation of DASCs to AT2 cells was observed by 25 dpi. In contrast, AT2 cells began proliferating from 7 dpi to replenish its population. Mass spectrometry and gene ontology analysis revealed prominent innate immune response at 7 dpi, which shifted towards adaptive immune responses by 15 dpi. Hence, proliferating AT2 cells but not DASCs contribute to AT2 cell regeneration following transition from innate to adaptive immune responses during the early phase of recovery from influenza pneumonia up to 25 dpi.
2020-04-17 | PXD014967 | Pride
Project description:Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses, suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However, a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia. We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus. Primary type II alveolar epithelial cells were isolated from human non-malignant lung tissue of three patients who underwent lung resection, and cells were differentiated to type I-like before use. Type I-like alveolar epithelial cells were mock infected, or infected with pdmH1N1 or seasonal H1N1 viruses at a multiplicity of infection (MOI) of two. Total RNA was extracted from cells after 8h post-infection, and gene expression profiling was performed using an Affymetrix Human Gene 1.0 ST microarray platform.
2010-10-06 | E-GEOD-24533 | biostudies-arrayexpress
Project description:Pandemic influenza H1N1 (pdmH1N1) virus causes mild disease in humans but occasionally leads to severe complications and even death, especially in those who are pregnant or have underlying disease. Cytokine responses induced by pdmH1N1 viruses in vitro are comparable to other seasonal influenza viruses, suggesting the cytokine dysregulation as seen in H5N1 infection is not a feature of the pdmH1N1 virus. However, a comprehensive gene expression profile of pdmH1N1 in relevant primary human cells in vitro has not been reported. Type I alveolar epithelial cells are a key target cell in pdmH1N1 pneumonia. We carried out a comprehensive gene expression profiling using the Affymetrix microarray platform to compare the transcriptomes of primary human alveolar type I-like alveolar epithelial cells infected with pdmH1N1 or seasonal H1N1 virus.
2010-10-06 | GSE24533 | GEO
Project description:Human disease caused by highly pathogenic avian influenza (HPAI) H5N1 can lead to a rapidly progressive viral pneumonia leading to acute respiratory distress syndrome. There is increasing evidence suggests a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. The key target cells for the virus in the lung are the alveolar epithelium and alveolar macrophages, and previous data has shown that compared to seasonal human influenza viruses, equivalent infecting doses of H5N1 viruses markedly up-regulate pro-inflammatory cytokines in both primary cell types in vitro. The dysregulation of H5N1-induced host responses is therefore important for understanding the viral pathogenesis. We used microarrays to analyze and compare the gene expression profiles in primary human macrophages after influenza A virus infection. Peripheral-blood leucocytes were separated from buffy coats of three healthy blood donors and cells were differentiated for 14 days before use. Differentiated macrophages were infected with H1N1 and H5N1 at a multiplicity of infection (MOI) of two. Total RNA was extracted from cells after 1, 3, and 6h post-infection, and gene expression profiling was performed using an Affymetrix Human Gene 1.0 ST microarray platform.
2009-10-31 | E-GEOD-18816 | biostudies-arrayexpress
Project description:Integrins facilitate intercellular movement and communication. Unlike the promiscuous activities of many integrins, β6 integrin is restricted to epithelia and partners exclusively with integrin αV to modulate acute lung injury (ALI). Given that ALI is a complication of respiratory infection, we used mice lacking β6 integrin (β6 KO) to probe the role of the epithelial layer in controlling the lung microenvironment during infection. We found β6 KO mice were protected from disease caused by influenza and Sendai virus infections. They were also protected from disease caused by Streptococcus pneumoniae infection alone and after prior influenza virus infection, the co-infection representing an often-lethal condition in humans. Resistance in the absence of epithelial β6 integrin was caused by intrinsic priming of the lung microenvironment by type I interferons through a mechanism involving transforming growth factor-β regulation. Expression of β6 on epithelia suppresses the production of interferons, providing an advantage to the pathogen. Acute inhibition of β6 function may therefore provide a means to improve outcomes in lung microbial infections. We used microarrays to explore the gene expression profiles differentially expressed in resident alveolar macrophage cells from wild-type and β6 integrin knockout mice. Cells were purified by sorting from lung digests. The comparison made was CD11c+, autofluorescent+ cells from wild-type controls to the dominant CD11c+, CD11b+, autofluorescent+ cells in the knockout. Note that conventional CD11c+ alveolar macrophages do not exist in the knockout mice.
2016-07-18 | E-GEOD-68802 | biostudies-arrayexpress
Project description:Alveolar macrophages maintain lung homeostasis and are critical for host defense to respiratory pathogens, including influenza virus. Yet how aging impacts alveolar macrophages remains unclear. Here, we found that aging reduces the proliferation and concentration of alveolar macrophages under basal conditions in mice. Transcriptomic analysis revealed that aging induces a down regulation in cell cycling pathways in alveolar macrophages. Functionally, aging impaired the capacity of alveolar macrophages to phagocytose in vivo, and also increased influenza virus-induced lung damage, morbidity and mortality. Depleting alveolar macrophages indicated that these cells were critical for accelerated mortality during influenza viral lung infection with aging. Adoptive transfer experiments demonstrated that aging impaired the ability of alveolar macrophages to reduce lung damage after influenza viral infection. Thus, our study has revealed that aging impairs alveolar macrophages to resolve damageand increases mortality after influenza viral infection.
2017-08-01 | GSE84901 | GEO
Project description:Community-acquired pneumonia is a widespread disease with significant morbidity and mortality. Alveolar macrophages are tissue-resident lung cells that play a crucial role in innate immunity against bacteria causing pneumonia. We hypothesized that alveolar macrophages display adaptive characteristics after resolution of bacterial pneumonia. We studied mice one to six months after self-limiting lung infection due to Streptococcus pneumoniae, the most common cause of bacterial pneumonia. Among the myeloid cells recovered from the lung, only alveolar macrophages showed long-term modifications of their surface marker phenotype. The remodeling of alveolar macrophages was: (i) long-lasting (still observed 6 months post infection), (ii) regionally localized (only observed in the affected lobe after lobar pneumonia), and (iii) associated with a macrophage-dependent enhanced lung protection to another pneumococcal serotype. Metabolomic and transcriptomic profiling revealed that alveolar macrophages of mice which recovered from pneumonia had new baseline activities and altered responses to infection. Thus, the enhanced lung protection after mild and self-limiting respiratory infection includes a profound remodeling of alveolar macrophages that is long-lasting, compartmentalized, and manifest across surface receptors, metabolites, and both resting and stimulated transcriptomes. We used microarrays to detail the global program of gene expression for mouse alveolar macrophages sorted from lungs that were naïve or infected more than a month previously, at rest and during an acute (4-hour) infection.
2020-04-17 | GSE133975 | GEO
Project description:Appropriate lung repair responses are essential to restore functional integrity and prevent severe disease phenotypes after injury. While macrophages are thought to contribute to repair, whether distinct subsets occupy particular niches and assume dedicated tasks to mediate host recovery post- injury remains unknown. Using an in vivo model of influenza A virus (IAV) infection in combination with single-cell and spatial transcriptomic analyses, bone marrow chimeras and monocyte fate-mapping, we found the transitional appearance of Ccr2-dependent monocyte-derived Ly6G+ macrophages (Ly6G Macs) after viral clearance. Ly6G Macs inhabited the alveolar spaces of regenerating perilesional areas, exhibited a unique ultrastructural morphology as well as a high metabolic potential. Using in vivo gene targeting and ex vivo wound healing assays, we found that Ly6G Macs could limit disease severity and promote alveolar regeneration via interleukin-4 receptor- and arginase-1-dependent mechanisms acting on type 2 alveolar epithelial cells. We also found evidence that similar macrophages existed in other models of lung injury and in the airways of virally-infected humans. Our study thus identifies perilesional alveolar Ly6G Macs as a spatially-restricted short-lived macrophage subset engaging a crosstalk with type 2 alveolar epithelial cells to promote alveolar regeneration and recovery post-injury, thus representing an attractive therapeutic target.
2024-05-30 | GSE244764 | GEO
Project description:Appropriate lung repair responses are essential to restore functional integrity and prevent severe disease phenotypes after injury. While macrophages are thought to contribute to repair, whether distinct subsets occupy particular niches and assume dedicated tasks to mediate host recovery post- injury remains unknown. Using an in vivo model of influenza A virus (IAV) infection in combination with single-cell and spatial transcriptomic analyses, bone marrow chimeras and monocyte fate-mapping, we found the transitional appearance of Ccr2-dependent monocyte-derived Ly6G+ macrophages (Ly6G Macs) after viral clearance. Ly6G Macs inhabited the alveolar spaces of regenerating perilesional areas, exhibited a unique ultrastructural morphology as well as a high metabolic potential. Using in vivo gene targeting and ex vivo wound healing assays, we found that Ly6G Macs could limit disease severity and promote alveolar regeneration via interleukin-4 receptor- and arginase-1-dependent mechanisms acting on type 2 alveolar epithelial cells. We also found evidence that similar macrophages existed in other models of lung injury and in the airways of virally-infected humans. Our study thus identifies perilesional alveolar Ly6G Macs as a spatially-restricted short-lived macrophage subset engaging a crosstalk with type 2 alveolar epithelial cells to promote alveolar regeneration and recovery post-injury, thus representing an attractive therapeutic target.
2024-05-30 | GSE244727 | GEO