ObjectivesWe herein aimed to explore whether growth arrest-specific 5 (GAS5) promotes M1 macrophage polarization in childhood pneumonia and to investigate the underlying mechanism. MethodsRelative GAS5 and miR-455-5p expression and suppressor of cytokine signaling 3 (SOCS3) messenger RNA level were examined using quantitative reverse transcription polymerase chain reaction. Protein expression of SOCS3 and the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway-related proteins was detected using western blot analysis. Luciferase activity assay was performed to test whether miR-455-5p could bind to GAS5 or SOCS3. The macrophage phenotype was determined using flow cytometry analysis and enzyme-linked immunosorbent assay. ResultsThe macrophage polarization toward the M2 phenotype was observed in peripheral blood from pneumonia children. Furthermore, GAS5 and SOCS3 expression were upregulated but miR-455-5p downregulated in human monocyte-derived macrophages from pneumonia children compared with the control group. Furthermore, GAS5 acted as a sponge for miR-455-5p to facilitate SOCS3 expression. Moreover, miR-455-5p mimic and SOCS3 knockdown significantly reversed the GAS5 overexpression-mediated suppression of the JAK2/STAT3 signaling and promotion of M1 polarization. ConclusionGAS5 promotes M1 macrophage polarization by acting as a competing endogenous RNA of miR-455-5p to facilitate SOCS3 expression in childhood pneumonia.