<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE329nnn/GSE329513/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329513</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Single-cell analysis reveals epithelial alarmin-associated immune architecture in pediatric refractory and rhinovirus-positive asthma</name><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.</description><dates><publication>2026/09/23</publication></dates><accession>GSE329513</accession><cross_references><GSM>GSM9705340</GSM><GSM>GSM9705333</GSM><GSM>GSM9705343</GSM><GSM>GSM9705332</GSM><GSM>GSM9705342</GSM><GSM>GSM9705331</GSM><GSM>GSM9705330</GSM><GSM>GSM9705341</GSM><GSM>GSM9705337</GSM><GSM>GSM9705336</GSM><GSM>GSM9705335</GSM><GSM>GSM9705334</GSM><GSM>GSM9705329</GSM><GSM>GSM9705339</GSM><GSM>GSM9705328</GSM><GSM>GSM9705338</GSM><GPL>24676</GPL><GSE>329513</GSE><taxon>Homo sapiens</taxon><PMID>[42750287]</PMID></cross_references></HashMap>