Introduction: There is increasing interest in the role of lipids in processes that modulate fibrosis. Specifically, some inherited surfactant dysfunction disorders result in pulmonary fibrosis. Surfactant consists of phospholipids and smaller quantities of neutral lipids such as cholesterol ester (CE). Tissue lipidomics on mouse bleomycin models demonstrates increased total lipid compared to control. Aims & objectives: To perform lipidomic analysis on human IPF lung tissue and assess the impact of specific lipids on human fibroblasts. Methods: Lung tissue from human IPF and control patients (n=10) were analysed for targeted quantitative measurement of >1,100 lipid species. Primary cell culture of human IPF and control fibroblasts was performed and cells were exposed to lipid species identified as increased on IPF tissue lipidomic analysis. Expression of alpha-smooth muscle actin (aSMA) and collagen 1 (Col1a1) were measured to assess for myofibroblast-like transition following lipid exposure. Results: There was an increase in pulmonary lipid content in patients with IPF compared to control (23.16nmol/mg vs. 18.66nmol/mg, p=0.0317). Specific increases were noted in 16:0, 20:4, and 22:6-containing lipids within both CE and PC species. Dose-related increases in aSMA and Col1a1 protein and RNA expression occur in human fibroblasts exposed to PC-16.0 and decreased expression when exposed to PC-20.4, CE 16.0, and CE 20.4. Conclusions: Abnormal lipid deposition is seen in IPF on lipidomic analysis. Specific lipid subgroups appear to impact fibroblast biology as seen by changes in aSMA and Col1a1 expression. Further investigation is still warranted to identify the specific action of lipids in fibrosis.