Abstract: ObjectiveTo explore the potential role of LINC01503 in the regulation of macrophage polarization and its function in the pathology of children asthma to achieve a better understanding of the pathology of asthma and find new strategies for asthma treatment. MethodsBlood was collected from asthmatic patients and healthy controls from August 26, 2017 to January 11, 2018 at Children's Hospital of Fudan University. PBMCs were separated from blood by gradient centrifuge. RT-qPCR was used for the detection of the expression of LINC01503 in PBMCs. LPS and IL-4 were used for the inducing of M1 and M2 polarization of macrophage separately. siRNA was used for knocking down LINC01503. RT-qPCR and Western blot were used for the detection of the effect of LINC01503 on the regulation of macrophage polarization. ResultsWe enrolled 28 patients of asthma and 46 healthy controls. Comparing with healthy controls，the expression of LINC01503 was significantly enhanced in asthmatic patients. LINC01503 was up-regulated in M2 macrophage but down-regulated in M1 macrophage. LINC01503 inhibited the M2 macrophage polarization indicated as the down regulation of CD206 and CD209. On the opposite, LINC01503 promoted the M1 macrophage polarization indicated as the up regulation of the expression of inflammatory mediators such as IL-6, TNF-α and CXCL10 through enhancing the phosphorylation of ERK. ConclusionLINC01503 was up-regulated in the asthmatic patients and it regulated macrophage polarization through a negative feedback loop.