OBJECTIVE To explore the expression of lubricin in the lumbar endplate and its association with Modic changes (MCs). METHODS Human endplate specimens harvested from patients undergoing surgery for thoracolumbar spine fractures ​or lumbar interbody fusion were divided into two groups: MCs group and normal group. Lubricin expression was examined by immunohistochemistry, and differences between the groups were analysed using quantitative polymerase chain reaction (qPCR). Lubricin expression and differences between endplates with MCs and normal endplates were confirmed using a rabbit model. In a final experiment, rabbit endplate chondrocytes were cocultured with Propionibacteria acnes (P. acnes) supernatant, and the expression of lubricin and endplate degeneration related genes were evaluated. In addition, the expression of matrix metalloproteinase 1(MMP-1), A disintegrin-like and metalloproteinase with thrombospondin type 5 motif (ADAMTS5) and inflammatory factors (Interleukin- 1β (IL-1β) and Interleukin-6 (IL-6)) were evaluated after lubricin overexpression. RESULTS Lubricin was found in human lumbar endplates and its expression was lower in the MCs group compared to the normal group. In the rabbit model, lubricin was also found in the endplate. In rabbits injected with P. acnes (the MCs group), lubricin expression of endplate decreased compared to the normal group. In the culture of rabbit endplate chondrocytes with P. acnes supernatant, the expression of lubricin, aggrecan, sox9 and collagen type-II decreased significantly, while that of MMP-1 and ADAMTS5 increased significantly. Moreover, lubricin overexpression could downregulate the expression of MMP-1, ADAMTS5 and inflammatory factors (IL-1β and IL-6) compared to negative control. CONCLUSIONS Lubricin is present in the lumbar endplate where it may have an anti-inflammatory role. P. acnes infection inhibits lubricin expression by cartilage endplate cells and this may facilitate the progression of MCs and endplate degeneration. Lubricin may have an anti-inflammatory role. P. acnes infection inhibits lubricin expression by cartilage endplate cells and this may facilitate the progression of MCs and endplate degeneration.