Alveolar macrophages serve as an early viral sponge inducing long-lived functional enhancement
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE215821 | GEO | 2026/06/01
REPOSITORIES: GEO
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Project description:Alveolar macrophages serve as an early viral sponge inducing long-lived functional enhancement
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Project description:Diagnosis of acute respiratory viral infection is currently based on clinical symptoms and pathogen detection. Use of host peripheral blood gene expression data to classify individuals with viral respiratory infection represents a novel means of infection diagnosis. We used microarrays to capture peripheral blood gene expression at baseline and time of peak symptoms in healthy volunteers infected intranasally with influenza A H3N2, respiratory syncytial virus or rhinovirus. We determined groups of coexpressed genes that accurately classified symptomatic versus asymptomatic individuals. We experimentally inoculated healthy volunteers with intranasal influenza, respiratory syncytial virus or rhinovirus. Symptoms were documented and peripheral blood samples drawn into PAXgene tubes for RNA isolation.
2009-08-06 | E-GEOD-17156 | biostudies-arrayexpress
Project description:Early life respiratory virus infections play an important role in shaping structural and immunological responses of the lung, leading to chronic airway disease Respiratory syncytial virus (RSV), a member of genus Orthopneumovirus, is an etiological agent in infant lower respiratory tract infections (LRTIs) producing substantial global morbidity. The mechanisms underlying how transient RSV infection produces long-term structural changes are unexplored. Although it is known that airway repair is mediated by expansion of parenchymal epithelial progenitors within discrete mesenchymal niches, the nature of these cells and how they are activated by viral infection are unknown. Herein, we explore the impact of RSV infection on trophic mesenchymal-basal epithelial interactions and the regenerative role of innate NFB/RelA signaling by its conditional knockout (CKO) in secretoglobin (Scgb1a1)-derived progenitors. We discovered that RSV-induced post viral lung disease (PVLD) induces expansion of parenchymal airspace and replacement of small bronchiolar and alveolar epithelium by tumor protein 63 (Trp63), Aquaporin-3 (Aqp3) and Integrin 4 (Itg4)-expressing cells. Single-cell RNA sequencing identifies populations of atypical alveolar type (AT)2 cells expressing both AT2 and AT1 markers. Mechanistically, we find this atypical progenitor expansion is prevented by RelA CKO in the Scgb1a1 lineage. A probabilistic analysis of the mesenchymal-epithelial cell-cell signaling network shows RSV induces an extensive network of epithelial-mesenchymal signaling through inflammatory platelet activated receptor (PAR), IL1/IL4 and stem-cell signaling by angiopoietin like (ANGPTL)-4 pathway. Interestingly, ANGPTL4 is normalized after Scgb1a1-directed RelA CKO. These data indicate RSV-PVLD is mediated, at least in part, by dysregulated mesenchymal-epithelial trophic signaling downstream of RelA activation in Scgb1a1-derived epithelial progenitors.
2026-04-01 | GSE291797 | GEO
Project description:Respiratory infections with RNA viruses such as respiratory syncytial virus (RSV) and influenza lead to significant morbidity and mortality. Using a natural rodent pathogen, Sendai virus (SeV), which is similar to RSV, mice made atopic with house dust mite survived a normally lethal SeV infection. Since we previously demonstrated a critical role for CD11c+ cells in the immune axis linking SeV to post-viral airway disease we posited that some of the protection against lethal SeV infection could be due to CD11c+ cells from atopic mice. Therefore, we performed RNA-seq analysis of CD11c+ cells isolated from atopic and non-atopic (NA) mouse lungs. While there were several dysregulated genes, one gene product whose expression was increased several-fold in atopic CD11c+ cells was neuregulin-1(NRG1) whose protein was found to be markedly elevated in the lungs and bronchoalveolar lavage fluid of atopic mice. When NRG1 was administered to naïve (non-atopic) mice it protected them from death with both SeV and mouse adapted influenza A virus (IAV). Survival was associated with reduced alveolar epithelium permeability and reduced phosphorylation of mixed lineage kinase domain-like (MLKL) protein indicating inhibition of necroptosis. In conclusion, our data demonstrate a unique function of NRG1 in respiratory viral infections by reducing alveolar leak, inhibiting epithelial necroptosis, and promoting homeostatic regulation of airway epithelium, all of which associate with markedly reduced mortality to the respiratory viral insult.
2025-04-15 | GSE281143 | GEO
Project description:Diagnosis of acute respiratory viral infection is currentlybased on clinical symptoms and pathogen detection. Use of host peripheral blood gene expression data to classify individuals with viral respiratory infection represents a novel means of infection diagnosis. We used microarrays to capture peripheral blood gene expression at baseline and time of peak symptoms in healthy volunteers infected intranasally with influenza A H3N2, respiratory syncytial virus or rhinovirus. We determined groups of coexpressed genes that accurately classified symptomatic versus asymptomatic individuals.
2009-08-06 | GSE17156 | GEO
Project description:Lower respiratory tract infections are among the top five leading causes of human death. Fighting these infections is therefore a world health priority. Searching for induced alterations in host gene expression shared by several relevant respiratory pathogens represent an alternative to identifying new targets for wide-range host-oriented therapeutics. With this aim, alveolar macrophages were independently infected with three unrelated bacterial (Streptococcus pneumoniae, Klebsiella pneumoniae and Staphylococcus aureus) and two dissimilar viral (respiratory syncytial virus and influenza A virus) respiratory pathogens which are nevertheless highly relevant for human health. Cells were also activated with bacterial lipopolysaccharide (LPS) as a prototypical pathogen-associated molecular pattern. Patterns of differentially expressed cellular genes shared by the indicated pathogens were searched by microarray analysis. Most of the commonly up-regulated genes were related to the innate immune response and/or apoptosis, with Toll-like, RIG-I-like and NOD-like receptors among the top ten signaling pathways with over-expressed genes. These results identify new potential broad-spectrum targets to fight the important human infections caused by the bacteria and viruses studied here.
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Project description:Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection
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Project description:Interferon Gamma signaling triggers dysplastic alveolar remodeling during respiratory viral infection
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Project description:We established a micro-patterned respiratory epithelial cell culture system in vitro. In this culture system, the iPSC-derived lung progenitor cells were differentiated into alveolar epithelial cells in a position-specific manner.
2024-02-29 | GSE236839 | GEO
Project description:The importance of alveolar type II epithelial cells (AEC II) in all aspects of the induction and regulation of respiratory immune responses has become increasing appreciated. We determined the genome-wide profile of gene expression in response to immune mediated airway inflammation. Overall, our results provide detailed description of specific AEC II gene expression under disease conditions. Differentially expressed genes of diverse molecular functions have been identified that may be critical for numerous physiologic activities, some of which may be currently unappreciated. Data obtained by such analysis will help to understand the function of these important immune cells in the respiratory system and may point out strategies for intervention in the progression of inflammatory diseases. We used microarrays to detail changes in the gene expression profile in alveolar type II epithelial cells during interstitial airway inflammation and identified a wide variety of differentially expressed genes during this process. Experiment Overall Design: Alveolar type II epithelial cells from the lung of healthy SPC-HA and diseased SPC-HAxTCR-HA mice were isolated by enzymatic tissue desintegration followed by one step negative selection using a MoFlow cell sorter. RNA was extracted and hybridization on Affymetrix microarrays was performed.
2008-06-13 | E-GEOD-5300 | biostudies-arrayexpress