Figure 6
High levels of IL-17A compromises gut epithelial barrier function and increases gut permeability.
(a) Morphine treatment increased FITC-dextran diffusion across the gut epithelium. The right panel was quantification of FITC intensity. *p < 0.05 (Student t test) (b) Quantification of FITC intensity in peritoneal lavage and whole blood *p < 0.05 (Student’s t test) (c) Anti-IL-17A injection reduced FITC-dextran diffusion across the gut epithelium in morphine-treated CLP animals. The right panel was quantification of FITC intensity. *p < 0.05 (Student’s t test) (d) Quantification of FITC intensity in peritoneal lavage and whole blood *p < 0.05 (Student’s t test) (e) H&E sections of small intestines from sham-operated or CLP animals treated with morphine or placebo. (f) H&E sections of small intestines from morphine-treated CLP animals injected with isotype control and anti-IL-17A. (g) TER was decreased by IL-17A in IEC-6 cell monolayer (H) The permeability of IEC-6 cell monolayer was increased in transwell system **p < 0.01 (ANOVA followed by Bonferroni’s t test) (n = 3) (i) ZO-1 organization in IEC6-cell monolayer treated by vehicle or 100 ng/ml IL-17A. Blue:DAPI Red:F-actin Green:ZO-1 White arrow indicates ZO-1 disruption.(j) H&E sections of small intestines from human patients.
