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A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE115824 | GEO | 2019/04/08

REPOSITORIES: GEO

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A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children [blood]

Project description:We leverage a systems-scale network analysis approach to demonstrate repertoires of cellular transcriptional pathways underlying loss of asthma control, and show how these pathways differ in viral associated and non-viral exacerbations.

2019-04-08 | GSE115823 | GEO

A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children [nasal]

2019-04-08 | GSE115770 | GEO

A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children

Project description:A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children

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A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children [blood]

Project description:A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children [blood]

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A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children [nasal]

Project description:A network of transcriptome modules demonstrates mechanistic pathways of both virus induced and non-viral asthma exacerbations in children [nasal]

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Transcriptome networks identify mechanisms of viral and nonviral asthma exacerbations in children.

Project description:Respiratory infections are common precursors to asthma exacerbations in children, but molecular immune responses that determine whether and how an infection causes an exacerbation are poorly understood. By using systems-scale network analysis, we identify repertoires of cellular transcriptional pathways that lead to and underlie distinct patterns of asthma exacerbation. Specifically, in both virus-associated and nonviral exacerbations, we demonstrate a set of core exacerbation modules, among which epithelial-associated SMAD3 signaling is upregulated and lymphocyte response pathways are downregulated early in exacerbation, followed by later upregulation of effector pathways including epidermal growth factor receptor signaling, extracellular matrix production, mucus hypersecretion, and eosinophil activation. We show an additional set of multiple inflammatory cell pathways involved in virus-associated exacerbations, in contrast to squamous cell pathways associated with nonviral exacerbations. Our work introduces an in vivo molecular platform to investigate, in a clinical setting, both the mechanisms of disease pathogenesis and therapeutic targets to modify exacerbations.

| S-EPMC6472965 | biostudies-literature

Predicting Severe Asthma Exacerbations in Children.

Project description: Not available

| S-EPMC5387707 | biostudies-literature

LPS binding protein and activation signatures are upregulated during asthma exacerbations in children

Project description:Asthma exacerbations in children are associated with respiratory viral infection and atopy, resulting in systemic immune activation and infiltration of immune cells into the airways. The gene networks driving the immune activation and subsequent migration of immune cells into the airways remains incompletely understood. Cellular and molecular profiling of PBMC was employed on paired samples obtained from atopic asthmatic children (n = 19) during acute virus-associated exacerbations and later during convalescence. Systems level analyses were employed to identify coexpression networks and infer the drivers of these networks, and validation was subsequently obtained via independent samples from asthmatic children. During exacerbations, PBMC exhibited significant changes in immune cell abundance and upregulation of complex interlinked networks of coexpressed genes. These were associated with priming of innate immunity, inflammatory and remodelling functions. We identified activation signatures downstream of bacterial LPS, glucocorticoids and TGFB1. We also confirmed that LPS binding protein was upregulated at the protein-level in plasma. Multiple gene networks known to be involved positively or negatively in asthma pathogenesis, are upregulated in circulating PBMC during acute exacerbations, supporting the hypothesis that systemic pre-programming of potentially pathogenic as well as protective functions of circulating immune cells preceeds migration into the airways. Enhanced sensitivity to LPS is likely to modulate the severity of acute asthma exacerbations through exposure to environmental LPS.

2023-09-12 | GSE96530 | GEO

Parental numeracy and asthma exacerbations in Puerto Rican children.

Project description:BackgroundPuerto Ricans share a disproportionate burden of childhood asthma in the United States. Little is known about the impact of low parental numeracy (a health literacy skill) on asthma morbidity in Puerto Rican children. Our objective was to examine whether low parental numeracy is associated with increased asthma morbidity in Puerto Rican children.MethodsThis was a cross-sectional study of 351 children with asthma, aged 6 to 14 years, living in San Juan, Puerto Rico. Parents of study participants completed a modified version of the Asthma Numeracy Questionnaire. Multivariate linear or logistic regression was used to examine the relation between low parental numeracy (defined as no correct answers in the modified Asthma Numeracy Questionnaire) and indicators of asthma morbidity (severe asthma exacerbations, core measures of asthma exacerbations, and lung function measures). All multivariate models were adjusted for age, sex, household income, reported use of inhaled corticosteroids in the previous 6 months, and exposure to secondhand tobacco smoke.ResultsLow parental numeracy was associated with increased odds of visits to the ED or urgent care for asthma (adjusted OR [aOR]=1.7, 95% CI=1.03-2.7, P=.04). The association between low parental numeracy and hospitalizations for asthma was significant only among children not using inhaled corticosteroids (aOR=2.8, 95% CI=1.4-5.6, P=.004). There was no association between low parental numeracy and use of systemic steroids or lung function measures.ConclusionsLow parental numeracy is associated with increased asthma morbidity in Puerto Rican children.

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Gene expression profiling of nasal swabs samples from children with asthma or wheezing exacerbations.

Project description:Nasal swab specimens were collected from children who presented to the emergency department with an acute exacerbation of asthma or wheeze. Samples were also collected from control subjects. Convalescent/quiescent samples were collected from children who were followed-up at least 6 weeks after an acute exacerbation of asthma or wheeze. Gene expression was profiled on microarrays.

2019-02-17 | GSE103166 | GEO

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