High-throughput screening of molecular markers for CTD-ILD

<bold>Background:</bold> Lung sampling is invasive and not practical in ILD, and the identification of other biological materials mirroring processes in the lung is needed. <bold>Objective:</bold> Determine nasal transcriptome in CTD-ILD as novel biomarkers. <bold>Methods:</bold> Nasal mucosa samples from patients with CTD-ILD and healthy controls from Oslo and UCLA were used to identify molecular markers for ILD across CTDs and for PPF. The nasal transcriptome was determined by NanoString technology, and gene expression and pathway analyses were conducted using ROSALIND software. <bold>Results:</bold> We included nasal mucosa samples from 39 CTD-ILDs and 10 healthy controls and identified 162 significant differentially expressed genes and several differentially activated signaling pathways between CTD-ILD patients and healthy controls (Figure). Several deregulated pathways were similar across the CTDs also previously identified in studies assessing RNA in lung tissue. All single diseases were enriched for IFN-type I (all log2FC| > 1.5-3.9), and IIM, RA and pSS-ILD for TH2 differentiation (log2FC| 1.9- > 2.6). Over 52 weeks, 10 (26%) patients showed PPF. We did not identify any significant upregulated genes compared to the non-progressive patients. <bold>Conclusion:</bold> We identified specific molecular markers for CTD-ILD using nasal transcriptomics from mucosa samples, also previously identified using RNAseq on lung tissues. This supports minimally invasive nasal swabs as novel biomarkers. <fig><object-id>erj;64/suppl_68/PA4267/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig>