The chromatin status fluctuates with effector and memory group 2 innate lymphoid cell (ILC2) responses. How this intricate coordination affects allergic lung inflammation remains unclear.We examined how the chromatin remodeler Brg1 regulates ILC2s in allergic lung inflammation.Acute lung allergic inflammation was induced with papain in wild-type, Il5Cre/+Smarca4f/f, Il5Cre/+Hif1af/f and Il5Cre/+Ldhaf/f mice. Secondary lung inflammation was induced with low-dose IL-33 in papain-primed Il5Cre/+Smarca4f/f mice. ATAC-seq, RNA-seq and Brg1 CUT&Tag analyses were performed on ILC2nav, ILC2eff, ILC2mem, IL-33 challenged Brg1-deficient ILC2, Brg1-deficient ILC2mem and human ILC2s treated with or without Brg1 inhibitor Compound14. ILC2 metabolism was analyzed with 13C glucose isotype tracing and metabolic flux, Seahorse and SCENITH assays. Compound14 was used to treat mouse and humanized mouse models of allergic lung inflammation.Brg1 expression was upregulated in asthma patients' ILC2s and was induced by IL-33. Brg1 promoted IL-5+ and IL-13+ ILC2 expansion and exacerbated both acute and secondary lung inflammation. Brg1 imprinted the chromatin landscape favoring aerobic glycolysis, the metabolic process reinforced in effector and memory ILC2s. Brg1-augmented Hif1a enhancer accessibility was a sustained epigenetic signature in memory ILC2s inherited from effector ILC2s, and Hif1α enhanced effector and memory ILC2 responses. Pharmacological inhibition of Brg1, rather than dexamethasone treatment, in acute phase alleviated secondary lung inflammation.Brg1 promotes the expansion of pathogenic effector and memory ILC2s and exacerbates allergic lung inflammation. Mechanistically, Brg1 increases the chromatin accessibility and transcription of Hif1a and Ldha, key factors reinforcing ILC2 glycolysis metabolism.Copyright © 2025. Published by Elsevier Inc.