Integrated analysis of mRNA and long noncoding RNA profiles in peripheral blood mononuclear cells of patients with bronchial asthma

BACKGROUND: Bronchial asthma is a heterogeneous disease with distinct disease phenotypes and underlying pathophysiological mechanisms. Long non-coding RNAs (lncRNAs) are involved in numerous functionally different biological and physiological processes. The aim of this study was to identify differentially expressed lncRNAs and mRNAs in patients with asthma and further explore the functions and interactions between lncRNAs and mRNAs. METHODS: Ten patients with asthma and 9 healthy controls were enrolled in this study. RNA was isolated from peripheral blood mononuclear cells. We performed microarray analysis to evaluate lncRNA and mRNA expression. The functions of the differentially expressed mRNAs were analyzed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses. A global signal transduction network was constructed to identify the core mRNAs. An lncRNA–mRNA network was constructed. Five mRNAs showing the greatest differences in expression levels or high degrees in the gene–gene functional interaction network, with their correlated lncRNAs, were validated by real-time quantitative polymerase chain reaction. RESULTS: We identified 2229 differentially expressed mRNAs and 1397 lncRNAs between the asthma and control groups. Kyoto Encyclopedia of Genes and Genomes pathway analysis identified many pathways associated with inflammation and cell survival. The gene–gene functional interaction network suggested that some core mRNAs are involved in the pathogenesis of bronchial asthma. The lncRNA–mRNA co-expression network revealed correlated lncRNAs. CXCL8, FOXO3, JUN, PIK3CA, and G0S2 and their related lncRNAs NONHSAT115963, AC019050.1, MTCYBP3, KB-67B5.12, and HNRNPA1P12 were identified according to their differential expression levels and high degrees in the gene–gene network. CONCLUSIONS: We identified the core mRNAs and their related lncRNAs and predicted the biological processes and signaling pathways involved in asthma. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12890-022-01945-9.