Increased resistance of GPR55-deficient mice to indomethacin-induced intestinal permeability. Increased resistance of GPR55-deficient mice to indomethacin-induced.

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Increased resistance of GPR55-deficient mice to indomethacin-induced intestinal permeability. Increased resistance of GPR55-deficient mice to indomethacin-induced intestinal permeability. (A to D) Serum FITC-dextran in GPR55 Het [DMSO, n = 4; indomethacin (Indo), n = 8] and KO (DMSO, n = 4; Indo, n = 8) mice (A), WT mice treated with vehicle (DMSO, n = 6; Indo, n = 13) or GPR55 antagonist CID16020046 (DMSO, n = 6; Indo, n = 13) (B), CCR9 WT (n = 6) and KO (n = 6) mice (C), or in WT (n = 12), GPR55 Het TCRδ KO (n = 13), and GPR55 KO TCRδ KO (n = 11) mice (D), all treated for 5 hours with vehicle (DMSO) or Indo and for 4 hours with FITC-dextran. (E) Immunofluorescence detection of TCRδ-eGFP and DAPI in GPR55 Het and KO mice treated with carrier (DMSO) or Indo for 4 hours. Scale bars, 50 μm. (F) Number of γδT IELs (number per 100-μm length) beneath (in PMS) or closely associated with the epithelium or in both compartments of GPR55 Het (DMSO, n = 6; Indo, n = 7) or KO (DMSO, n = 8; Indo, n = 9) mice treated with DMSO on Indo as in (E). (G) Percentage of γδT IEL in close association with the epithelium. (H) Number of γδT IEL in GPR55 Het (DMSO, n = 7; Indo, n = 11) and KO (DMSO, n = 9; Indo, n = 9) mice 4 hours after DMSO or Indo treatment as determined by flow cytometry. ***P < 0.001, **P < 0.01, *P < 0.05, n.s. P > 0.05 by Student’s t test (A to C and F to H) or one-way ANOVA (D). Hayakazu Sumida et al. Sci. Immunol. 2017;2:eaao1135 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works