RNA-Seq data from epiphyseal growth plates of young male rats, healthy control rats and dextran sodium sulfate (DSS) induced colitis treated rats
Growth failure is a major complication of pediatric inflammatory bowel disease (IBD), a condition whose prevalence has risen sharply over recent decades. Despite advances in medical therapy, linear growth impairment often persists. This underscores the urgent need to elucidate how chronic inflammation disrupts skeletal development at the epiphyseal growth plate (EGP), the central driver of longitudinal bone growth. Our study proposes a novel mechanism, involving the activation of ELANE, a serine proteinase previously shown to be secreted by neutrophils in response to inflammatory stimuli. We report for the first time that EGP chondrocytes express ELANE, with significant upregulation observed in DSS-induced colitis and in ATDC5 cells exposed to LPS. The concomitant induction of ELANE and MMP13 indicates a direct catabolic effect on the extracellular matrix, leading to impaired growth plate function. While ELANE is well established in cartilage degradation and bone remodeling in rheumatoid arthritis and osteoarthritis, its expression in the EGP and its role in growth impairment during IBD represent novel findings. These findings open new perspectives on inflammation-driven growth impairment in pediatric IBD, highlight ELANE as a promising therapeutic target to preserve skeletal development.