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Influenza-induced activation of recruited alveolar macrophages during the early inflammatory phase drives lung injury and lethality

ABSTRACT: Influenza-induced activation of recruited alveolar macrophages during the early inflammatory phase drives lung injury and lethality

PROVIDER: PRJNA757241 | ENA |

REPOSITORIES: ENA

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Influenza-induced activation of recruited alveolar macrophages during the early inflammatory phase drives lung injury and lethality

Project description:we identify gene expression patterns associated with three distinct phases (Infiltrating, Early Inflammatory, Late Inflammatory) in the influenza A virus response of recruited alveolar macrophages. In the Early Inflammatory phase, recruited macrophages begin expressing pro-inflammatory genes, driving cytokine-mediated lung damage and contributing to the morbidity observed in influenza-infected wild-type mice. In mice lacking vimentin (Vim-/-), genes associated with the Early Inflammatory phase are suppressed, while the expression of the Infiltrating Phase genes is maintained, which is associated with protection from influenza-induced injury. Using a bone-marrow chimera mouse model, we validate that Vim-/- recruited alveolar macrophages are sufficient to confer protection from influenza-induced mortality. Our results define the temporal dynamics of gene expression in recruited alveolar macrophages, which shape the host response to infection with respiratory viruses.

2024-08-01 | GSE182637 | GEO

Gene expression in murine alveolar macrophage: effect of aging and influenza infection

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

Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells

Project description:Examine differences in Type-1 alveolar epithelial cells with and without alveolar macrophages during influenza infection

2017-01-06 | GSE93085 | GEO

Transcription profiling of mouse peripheral blood and alveolar recruited mononuclear phagocytes in Pam3CSK4 treated animals

Project description:Aim of this project was to examine the global gene expression profiles of mononuclear phagocytes recruited from peripheral blood to the alveolar space following alveolar deposition of the TLR2-ligand Pam3CSK4 in transgenic CX3CR1+/GFP mice. Experiment Overall Design: Alveolar macrophages (AM) and peripheral blood monocytes (PBM) were isolated from broncho-alveolar lavages and from blood, respectively, using FACS. Expression profiles from AM and PBM of the same mice were compared on the same slides. Each labeled RNA sample contained RNA pooled from six individuals. Four pairs of RNA from corresponding AM and PBM pools were hybridized, giving a total amount of 24 individual mice analyzed. Two hybridizations were performed with AM labeled with Cy3 and PBM with Cy5, two hybridizations were performed with swaped dyes.

2009-01-09 | E-GEOD-11978 | biostudies-arrayexpress

Gene expression profiling of peripheral blood and alveolar recruited mononuclear phagocytes in Pam3CSK4 treated mice

2009-01-01 | GSE11978 | GEO

RNA-seq of mouse alveolar macrophages from control and Influenza A virus infected animals

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

Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

Project description:Lung macrophages mediate helminth resistance through differential activation of recruited monocyte-derived alveolar macrophages and arginine depletion

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Expression data of influenza A-infected human type I-like alveolar epithelial cells

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

Transcriptome analysis of a novel alveolar porcine epithelial cells line infected with different live attenuated Influenza Viruses

Project description:The project aim at studying transcriptional changes by BRB-seq of porcine alveolar epithelial cells line infected with wild type influenza virus compared to live attenuated influenza viruses. In addition, primary porcine nasal epithelial cells was also added to be able to compare how the alveolare epithelial cells line compare to primary cells. Finally, additional positive control including procine alveolar epithelial cells stimulated with Poly I:C or infected with IFN inducing Sendei virus was added.

2023-08-31 | E-MTAB-13128 | biostudies-arrayexpress

Transcriptomics of isolated alveolar macrophages from WT and CD47 deficient mice upon influenza A virus infection

Project description:CD47 is an ubiquitously expressed surface molecule that has a significant impact on immune responses. However, its role for antiviral immunity is not fully understood. We can show that CD47 has an inhibitory role in influenza virus defense, since CD47-deficient mice (CD47-/-) display an increased viral clearance during influenza virus infection. This effect is strongly associated with alveolar macrophages, yet the underlying mechanisms are unclear. Thus, to assess the precise impact of CD47 on antiviral action of alveolar macrophages, transcriptional analysis of ex vivo isolated alveolar macrophages from CD47-/- and WT mice were performed isolated 3dpi. Surprisingly, instead of classical antiviral mediators, an increased expression of both hemoglobin α and hemoglobin β was found in CD47 deficient compared to WT alveolar macrophages upon influenza A virus infection. Importantly, antiviral activity of hemoglobin was already shown for other viruses and thus, CD47 might limit influenza virus defense via the regulation of hemoglobin, which could act as a modulator of the antiviral immune response during the infection.

2022-12-09 | GSE201825 | GEO

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