Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA144385 | ENA |
REPOSITORIES: ENA
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Project description:Current prophylactic and therapeutic strategies targeting human influenza viruses include vaccines and antivirals. Given variable rates of vaccine efficacy and antiviral resistance, alternative strategies are urgently required to improve disease outcomes. Here we describe the use of HiSeq deep sequencing to analyze host gene expression in primary human alveolar epithelial type II (ATII) cells infected with highly pathogenic avian influenza H5N1 virus. We employed primary human ATII cells isolated from normal human lung tissue donated by patients that underwent lung resection. Human host gene expression following HPAI H5N1 virus (A/Chicken/Vietnam/0008/04) infection of primary ATII cells was analyzed using Illumina HiSeq deep sequencing.
2018-10-09 | GSE119767 | GEO
Project description:Airway epithelial cells and macrophages differ markedly in their responses to influenza A virus (IAV) infection. To investigate transcriptional responses underlying these differences, purified subsets of type II airway epithelial cells (ATII) and alveolar macrophages (AM) recovered from the lungs of mock- or IAV-infected mice were subjected to RNA sequencing. In the absence of infection, AM predominantly expressed genes related to immunity whereas ATII expressed genes consistent with their physiological roles in the lung. Following IAV infection, AM almost exclusively activated cell-intrinsic antiviral pathways that were dependent on interferon regulatory factor (IRF)3/7 and/or type I interferon (IFN) signaling. In contrast, IAV-infected ATII activated a broader range of physiological responses, including cell-intrinsic antiviral pathways, which were both independent and dependent on IRF3/7 and/or type I IFN. These data suggest that transcriptional profiles hardwired during development could be a major determinant underlying the different responses of ATII and AM to IAV infection.
2018-12-20 | GSE115904 | GEO
Project description:Respiratory infections, like the current pandemic SARS-CoV-2 virus, target the epithelial cells in the respiratory tract. However, alveolar macrophages (AMs) are tissue-resident macrophages located within the alveoli of the lung and they play a key role in the early phases of an immune response to respiratory infections. We expect that AMs are the first immune cells to encounter the SARS-CoV-2 and therefore their reaction to SARS-CoV-2 infection will have a profound impact upon the outcome of the infection. Interferons (IFNs) are antiviral cytokines and the first cytokine produced upon viral infection. Here, we challenge AMs with SARS-CoV-2 and to our surprise find that the AMs are incapable of recognising SARS-CoV-2 and produce IFN. This is in contrast to respiratory pathogens, such as influenza A virus and Sendai virus. Callenge of AMs with those viruses resulted in a robust IFN response. The absence of IFN production by AMs upon challenge could explain the initial asymptotic phase of SARS-CoV-2 infections and argues against the AMs as the source of proinflamatory cytokines later in infection.
2020-10-20 | PXD021685 | Pride
Project description:Based on the observations that influenza infection led to behavioral changes in alveolar macrophages (AMs), we performed an RNAseq experiment to delineate global gene expression changes that occurred in the AM population after influenza infection versus a control (non-infected) population.
2020-08-31 | E-MTAB-9429 | biostudies-arrayexpress
Project description:This project is based upon the fundamental observation that alveolar macrophage-derived extracellular vesicles (AM-EVs), when internalized by neighboring epithelial cells, inhibit their infection by influenza virus. This inhibitory activity of AM-EVs is abolished when AMs are treated with cigarette smoke extract (CSE). We chose to survey the AM-EV proteome in an effort to identify candidate proteins whose abundance within EVs was downregulated by CSE treatment of AMs, thus explaining the ability of CSE to abrogate the inhibitory activity against influenza.
2020-06-09 | PXD019528 | Pride
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:We used RNA sequencing to comprehensively map the expression of coding and non-coding RNAs in primary human alveolar epithelial type II cells (AECIIs), alveolar macrophages (AMs), human lung tissue, and the epithelial cell line A549 during infection with IAV strain H3N2 Panama
2022-12-16 | GSE206606 | GEO
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:Respiratory viral infections reprogram pulmonary macrophages with altered anti-infectious functions. However, the potential function of virus-trained macrophages in antitumor immunity in the lung, a preferential target of both primary and metastatic malignancies, is not well understood. Using mouse models of influenza and lung metastatic tumors, we show here that influenza trains respiratory mucosal-resident alveolar macrophages (AMs) to exert long-lasting and tissue-specific antitumor immunity. Trained AMs infiltrate tumor lesions and have enhanced phagocytic and tumor cell cytotoxic functions, which are associated with epigenetic, transcriptional and metabolic resistance to tumor-induced immune suppression. Generation of antitumor trained immunity in AMs is dependent on interferon-γ and natural killer cells. Notably, human AMs with trained immunity traits in non-small cell lung cancer tissue are associated with a favorable immune microenvironment. These data reveal a function for trained resident macrophages in pulmonary mucosal antitumor immune surveillance. Induction of trained immunity in tissue-resident macrophages might thereby be a potential antitumor strategy.
2023-01-09 | GSE222148 | GEO
Project description:Respiratory viral infections reprogram pulmonary macrophages with altered anti-infectious functions. However, the potential function of virus-trained macrophages in antitumor immunity in the lung, a preferential target of both primary and metastatic malignancies, is not well understood. Using mouse models of influenza and lung metastatic tumors, we show here that influenza trains respiratory mucosal-resident alveolar macrophages (AMs) to exert long-lasting and tissue-specific antitumor immunity. Trained AMs infiltrate tumor lesions and have enhanced phagocytic and tumor cell cytotoxic functions, which are associated with epigenetic, transcriptional and metabolic resistance to tumor-induced immune suppression. Generation of antitumor trained immunity in AMs is dependent on interferon-γ and natural killer cells. Notably, human AMs with trained immunity traits in non-small cell lung cancer tissue are associated with a favorable immune microenvironment. These data reveal a function for trained resident macrophages in pulmonary mucosal antitumor immune surveillance. Induction of trained immunity in tissue-resident macrophages might thereby be a potential antitumor strategy.
2023-01-09 | GSE222149 | GEO