Analyzing the variance in protein expression profiles between patients diagnosed with idiopathic pulmonary fibrosis (IPF) and those with non-IPF interstitial lung diseases (ILD)

<bold>Background:</bold> Fibrotic interstitial lung diseases (F-ILDs) encompass a diverse array of disorders characterized by lung scarring or fibrosis. Among these, idiopathic pulmonary fibrosis (IPF) represents a primary category of F-ILD, and together with non-IPF ILD, they share similar mechanistic pathways leading to lung fibrosis. However, their pathophysiology is distinct. Our objective is to investigate the variances in protein expression profiles between IPF and non-IPF ILD among Taiwanese patients. <bold>Methods:</bold> A cross-sectional analysis was performed on 88 F-ILD patients, including 22 with IPF and 66 with non-IPF ILD. Using the O-link inflammation panel, we assessed the plasma levels of 96 inflammation-associated proteins across both patient groups. <bold>Results:</bold> Patients in the IPF group were older, predominantly male, with a history of smoking, and frequently presented basal crackles and clubbing of the fingers, alongside higher serum ferritin levels. Proteomic assessments showed elevated levels of 20 proteins in the IPF group, involved in pathways such as innate and adaptive immunity (e.g., ADA, CD5, CD8A, TNF, IL-10RB, IL6), chemotaxis (CXCL6, CXCL9, CCL23), cell growth (HGF, STAMBP, VEGFA, IL-24), extracellular matrix remodeling (MMP-1, MMP-10, uPA), among others (CDCP1, PD-L1, OPG, FGF-19), while the TWEAK protein was reduced. <bold>Conclusion:</bold> Our study identifies unique biomarkers differentiating IPF from non-IPF ILD, suggesting that a specific proteomic signature could enhance the differential diagnosis of F-ILD.