γδ T cells exacerbate intestinal fibrosis in mice with experimental colitis via activation of the CD73-adenosine receptor-cyclic AMP signaling pathway

Figure 4 Inhibition of CD73 attenuated intestinal fibrosis. A: Experimental scheme of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced intestinal fibrosis model. PSB-12379 were intraperitoneally injected after TNBS administration; B: Quantitative polymerase chain reaction analysis of the expression of CD73 gene in mice treated with TNBS and TNBS + PSB-12379 injection. Normal colon tissues were used as the control (n = 3 in each group). Data are presented as relative mRNA levels normalized to β-actin; C: The 5’-nucleotidase activity of CD73 in each group, normal colon tissues were used as the control (n = 3); D: The concentrations of ATP in the colon tissues; E: Body weight changes in the mice administrated with TNBS or TNBS + PSB-12379 during the experimental period (n = 5); F: Disease activity index score evaluated in the mice treated with TNBS or TNBS + PSB-12379 (n = 5); G: The representative image for hematoxylin and eosin, Masson staining and immunohistochemistry staining of TCR in the colon tissues in the mice treated with TNBS or TNBS + PSB-12379. Orange arrow indicated areas of immune cell infiltration. Scale bars: 100 μm or 50 μm; H: Quantification of immunohistochemistry staining (Figure 4G), described as mean optical density; I: The concentrations of hydroxyproline levels in the serum at week 14 (n = 3); J: The levels of hyaluronic acid, type IV collagen, laminin, and procollagen III in the serum at week 14 (n = 3). Data were presented as mean ± SD. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. TNBS: 2,4,6-trinitrobenzenesulfonic acid; NT5E: 5’-nucleotidase; DAI: Disease activity index; H&E: Hematoxylin and eosin; HA: Hyaluronic acid; IV-C: Type IV collagen; LN: Laminin; PCIII: Procollagen III.