Our findings indicated that pro-inflammatory and pro-fibrotic mediators are increased at the baseline in BSMCs from both asthma and COPD, and that TLR3 agonist polyI:C, significantly upregulated IL-6, IFN-β1, CCL2, FN1 and COL1A1 expressions in BSMCs (Figures 3A–F and 5A–D). The gene discussed is IFNB1; the disease is asthma.