{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329513/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329513"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell analysis reveals epithelial alarmin-associated immune architecture in pediatric refractory and rhinovirus-positive asthma","description":"Background: Asthma in children is increasingly recognized as biologically distinct from adult disease, yet the cellular organization underlying refractory asthma and virus-associated exacerbation remains poorly defined. In particular, how chronic airway remodeling and acute viral responses are integrated within the pediatric airway microenvironment is not well understood. Methods:Children with asthma were classified into refractory asthma (defined according to Global Initiative for Asthma criteria) and rhinovirus-positive asthma (defined by qPCR-confirmed rhinovirus infection). Bronchoalveolar lavage fluid samples from children with refractory asthma (n = 5), rhinovirus-positive asthma (n = 4) and healthy controls (n = 6) were subjected to single-cell RNA sequencing, followed by integrative bioinformatic analysis and cross-age comparison with adult asthma datasets. Controls were obtained from individuals undergoing bronchoscopy for non-inflammatory indications and lacked a history of atopy or airway inflammatory disease. Results: Pediatric refractory asthma showed increased epithelial cell representation, elevated epithelial alarmin–related gene expression, enhanced chemokine and interferon-stimulated gene signatures, and increased expression of remodeling-associated genes. Cell–cell communication analysis identified enhanced macrophage-to-epithelium signaling mediated through FN1–CD44/αVβ integrin interactions. Rhinovirus-positive asthma exhibited a more pronounced inflammatory profile, characterized by increased T-cell abundance, enhanced chemokine and interferon responses, and strengthened CTL–macrophage communication via the CCL5–CCR1 axis. Cross-age comparison indicated relatively higher epithelial alarmin–associated features in pediatric asthma and stronger chemokine-associated signatures in adult asthma.","dates":{"publication":"2026/09/23"},"accession":"GSE329513","cross_references":{"GSM":["GSM9705340","GSM9705333","GSM9705343","GSM9705332","GSM9705342","GSM9705331","GSM9705330","GSM9705341","GSM9705337","GSM9705336","GSM9705335","GSM9705334","GSM9705329","GSM9705339","GSM9705328","GSM9705338"],"GPL":["24676"],"GSE":["329513"],"taxon":["Homo sapiens"],"PMID":["[42750287]"]}}