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. Author manuscript; available in PMC: 2018 Jun 8.
Published in final edited form as: Sci Immunol. 2017 Dec 8;2(18):eaao1135. doi: 10.1126/sciimmunol.aao1135

Fig. 6. Increased resistance of GPR55-deficient mice to indomethacin induced intestinal permeability.

Fig. 6

(A–D) Serum FITC-dextran in GPR55 Het (DMSO, n=4; 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 indomethacin (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 indomethacin (Indo) for 4 hours. Scale bars, 50μm. (F) Number of γδT IELs (number per 100um 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, B, C, F, G, H) or one-way ANOVA (D).