Acute viral bronchiolitis
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ABSTRACT:
PROVIDER: PRJNA450428 | ENA |
REPOSITORIES: ENA
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Project description:Acute viral bronchiolitis (PBMC)
| PRJNA450430 | ENA
Project description:Acute viral bronchiolitis (NMS)
| PRJNA450429 | ENA
Project description:Background: A subset of infants are hyper-susceptible to severe/acute viral bronchiolitis (AVB), for reasons unknown. Purpose: To characterise the cellular/molecular mechanisms underlying infant AVB in circulating cells/local airways tissues. Methods: PBMC and nasal mucosal scrapings (NMS) were obtained from Infants (<18mths) and children (1.5-5yrs) during AVB and post-convalescence. Immune response patterns were profiled by multiplex analysis of plasma cytokines, flow cytometry, and transcriptomics (RNA-Seq). Molecular profiling of group-level data utilised a combination of upstream regulator and coexpression network analysis, followed by individual subject-level data analysis employing personalised N-of-1-pathways methodology. Results: Group-level analyses demonstrated that infant PBMC responses were dominated by monocyte-associated hyper-upregulated type I interferon signalling/pro-inflammatory pathways (drivers: TNF, IL6, TREM1, IL1B), versus a combination of inflammation (PTGER2, IL6) plus growth/repair/remodelling pathways (ERBB2, TGFB1, AREG, HGF) coupled with Th2 and NK-cell signalling in children. Age-related differences were not attributable to differential steroid usage or variations in underlying viral pathogens. Nasal mucosal responses were comparable qualitatively in infants/children, dominated by interferon types I-III, but the magnitude of upregulation was higher in infants (range 6-48-fold) than children (5-17-fold). N-of-1-pathways analysis confirmed differential upregulation of innate immunity in infants and NK cell networks in children, and additionally demonstrated covert AVB response sub-phenotypes that were independent of chronological age. Conclusions: Dysregulated expression of interferon-dependent pathways following respiratory viral infections is a defining immunophenotypic feature of AVB-susceptible infants and a subset of children. Susceptible subjects appear to represent a discrete subgroup who cluster based on (slow) kinetics of postnatal maturation of innate immune competence.
2018-12-24 | GSE113209 | GEO
Project description:Background: A subset of infants are hyper-susceptible to severe/acute viral bronchiolitis (AVB), for reasons unknown. Purpose: To characterise the cellular/molecular mechanisms underlying infant AVB in circulating cells/local airways tissues. Methods: PBMC and nasal mucosal scrapings (NMS) were obtained from Infants (<18mths) and children (1.5-5yrs) during AVB and post-convalescence. Immune response patterns were profiled by multiplex analysis of plasma cytokines, flow cytometry, and transcriptomics (RNA-Seq). Molecular profiling of group-level data utilised a combination of upstream regulator and coexpression network analysis, followed by individual subject-level data analysis employing personalised N-of-1-pathways methodology. Results: Group-level analyses demonstrated that infant PBMC responses were dominated by monocyte-associated hyper-upregulated type I interferon signalling/pro-inflammatory pathways (drivers: TNF, IL6, TREM1, IL1B), versus a combination of inflammation (PTGER2, IL6) plus growth/repair/remodelling pathways (ERBB2, TGFB1, AREG, HGF) coupled with Th2 and NK-cell signalling in children. Age-related differences were not attributable to differential steroid usage or variations in underlying viral pathogens. Nasal mucosal responses were comparable qualitatively in infants/children, dominated by interferon types I-III, but the magnitude of upregulation was higher in infants (range 6-48-fold) than children (5-17-fold). N-of-1-pathways analysis confirmed differential upregulation of innate immunity in infants and NK cell networks in children, and additionally demonstrated covert AVB response sub-phenotypes that were independent of chronological age. Conclusions: Dysregulated expression of interferon-dependent pathways following respiratory viral infections is a defining immunophenotypic feature of AVB-susceptible infants and a subset of children. Susceptible subjects appear to represent a discrete subgroup who cluster based on (slow) kinetics of postnatal maturation of innate immune competence.
2018-12-24 | GSE113210 | GEO
Project description:Human respiratory syncytial virus (HRSV) is the main cause of bronchiolitis during the first year of life, but other viruses such as rhinovirus also occur and are clinically indistinguishable. In hospitalized infants with bronchiolitis, the analysis of the peripheral blood mononuclear cells (PBMC) gene expression might be useful for identification the etiologies caused by HRSV and human rhinovirus (HRV) and to the development of future tests, as well as to elucidate the pathogenic mechanisms triggered by different viral agents and new therapeutic possibilities. In this study, we conducted a comparative global gene expression analysis of infants with acute viral bronchiolitis infected by HRSV (HRSV group) or HRV (HRV group).
2019-03-19 | GSE124124 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2018-12-24 | GSE113211 | GEO
Project description:Regulatory T (Treg) cells act as terminators in the case of T cell immunity during the acute phase of viral infection. However, their roles in chronic viral infection are not completely understood. We compared the phenotype and function of Treg cells during acute and chronic viral infection using lymphocytic choriomeningitis virus-infected mouse models. Chronic infection, unlike acute infection, led to induction of Treg cells and upregulation of various inhibitory receptors. Treg cells isolated from chronically infected mice (chronic Treg cells) displayed greater suppressive capacity for inhibiting T cell proliferation and subsequent cytokine production than those from naM-CM-/ve (naive Treg cells) or acutely infected mice (acute Treg cells). These gene expression profiles provided evidence that chronic Treg cells display characteristics distinct from either naive or acute Treg cells. Mouse splenic CD4+CD25+ regulatory T cells were analyzed at 0 day and 16 day after acute or chronic viral infection with LCMV Arm or CL13, respectively.
2014-12-05 | E-GEOD-63876 | biostudies-arrayexpress
Project description:Early life respiratory viral infections and atopic characteristics are significant risk factors for the development of childhood asthma. It is hypothesized that repeated respiratory viral infections might induce structural remodeling by interfering with the normal process of lung maturation; however, the specific molecular processes that mediate these developments are not understood. To define relevant molecular pathways, we used a well-established Sendai virus infection model in weanling rats to compare transcriptome signatures between a post-infection asthma prone susceptible strain (BN) and a post-infection asthma resistant strain (F344). Specific to this weanling model and not described in adult models, Sendai virus infection in the susceptible strain resulted in morphological abnormalities in distal airways that persist into adulthood, suggesting a disruption of normal lung growth. Gene expression data from infected and control lungs across five time points indicated that specific features of the immune response following viral infection were heightened and prolonged in lungs from BN compared with F344 rats. These features included an increase in macrophage cell number and related gene expression, which then transitioned to an increase in mast cell number and related gene expression. In contrast to the heightened immune response in infected BN lungs, infected F344 lungs displayed more efficient re-epithelialization. We conclude that the structural defects that developed and persisted in infected BN but not F344 lungs were preceded by a pronounced macrophage and mast cell response to viral infection acting in parallel with an inadequate re-epithelialization. For each of the five time points, one array was run for each of the four conditions (F344 control, BN control, F344 virus, BN virus) with 15 individual smaples pooled on each array.
2013-10-01 | E-GEOD-51267 | biostudies-arrayexpress
Project description:Early life respiratory viral infections and atopic characteristics are significant risk factors for the development of childhood asthma. It is hypothesized that repeated respiratory viral infections might induce structural remodeling by interfering with the normal process of lung maturation; however, the specific molecular processes that mediate these developments are not understood. To define relevant molecular pathways, we used a well-established Sendai virus infection model in weanling rats to compare transcriptome signatures between a post-infection asthma prone susceptible strain (BN) and a post-infection asthma resistant strain (F344). Specific to this weanling model and not described in adult models, Sendai virus infection in the susceptible strain resulted in morphological abnormalities in distal airways that persist into adulthood, suggesting a disruption of normal lung growth. Gene expression data from infected and control lungs across five time points indicated that specific features of the immune response following viral infection were heightened and prolonged in lungs from BN compared with F344 rats. These features included an increase in macrophage cell number and related gene expression, which then transitioned to an increase in mast cell number and related gene expression. In contrast to the heightened immune response in infected BN lungs, infected F344 lungs displayed more efficient re-epithelialization. We conclude that the structural defects that developed and persisted in infected BN but not F344 lungs were preceded by a pronounced macrophage and mast cell response to viral infection acting in parallel with an inadequate re-epithelialization.
2013-10-01 | GSE51267 | GEO