<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/GSE326nnn/GSE326017/</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=GSE326017</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Microbial Ecological Instability And Non-Linear Host Interactions Shape Airway Inflammation In HIV-Associated COPD [scRNA-seq]</name><description>Chronic Obstructive Pulmonary Disease (COPD) is increasingly prevalent among people infected with human immunodeficiency virus (HIV) in sub-Saharan Africa, yet the ecological and immunological mechanisms linking airway microbes to mucosal inflammation remain unclear. We performed multi-omics profiling in adults from rural Uganda stratified by their HIV and COPD status, integrating sputum microbiome sequencing, outer membrane vesicle quantification, cytokine profiling, cytometry by time-of flight immunophenotyping, and bulk and single-cell transcriptomics with bronchoalveolar lavage-guided deconvolution. Temporal ecological dynamics predominantly shaped airway microbial structure, although disease-modified instability patterns, particularly Haemophilus enrichment and altered trajectories of Staphylococcus, Gemella, and Moraxella, were detectable in HIV+/COPD+ individuals. In contrast, host immune phenotypes showed disease-linked remodeling: HIV and COPD were associated with activation of NF-κB, IL-17, chemokine, TLR, NOD, and antiviral pathways and with compartment-specific transcriptional shifts across sputum, bronchoalveolar lavage, and blood. Integrative modeling revealed discrete, non-linear microbe-immune interaction modules rather than broad dysbiosis, indicating that specific taxa engage defined inflammatory circuits. Together, these findings suggest that HIV-associated COPD reflects immune-skewed mucosal remodeling in which the airway microbiome functions as a selective, temporally dynamic modulator of inflammatory states rather than a globally disrupted community.</description><dates><publication>2026/09/05</publication></dates><accession>GSE326017</accession><cross_references><GSM>GSM9619289</GSM><GSM>GSM9619293</GSM><GSM>GSM9619294</GSM><GSM>GSM9619291</GSM><GSM>GSM9619292</GSM><GSM>GSM9619290</GSM><GPL>24676</GPL><GSE>326017</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>