Editorial
Copyright ©2014 Baishideng Publishing Group Inc.
World J Gastroenterol. Aug 28, 2014; 20(32): 11023-11032
Published online Aug 28, 2014. doi: 10.3748/wjg.v20.i32.11023
Figure 1
Figure 1 Prevalence of sinonasal disease in inflammatory bowel disease patients. Reproduced with permission from reference Book et al[34]. CD: Crohn’s disease.
Figure 2
Figure 2 Immune privilege in the gut consists of tolerance to dietary antigens and to commensal microbes[49]. Reproduced with permission from reference Iweala et al[49]. CD: Crohn’s disease; UC: Ulcerative colitis; TNF-α: Tumor necrosis factor-α; IL: Interleukin; IFN: Interferon.
Figure 3
Figure 3 Histologic analysis of the colon in C57BL/6 mice. A: Normal architecture of the colonic mucosa from mice treated with 50% ethanol alone; B: Erosions of the epithelium, distortion of crypts, loss of goblet cells, and massive mononuclear cell infiltration in lamina propria in mice after administration of trinitrobenzene (TNBS); C-E: TNBS-induced colitis is dose-dependently improved by curcumin. Mice were treated with 0.5% (C), 2.0% (D), or 5.0% (E) curcumin just after administration of TNBS; F-H: Mice were treated with 2% curcumin in preventive mode (F), early therapeutic mode (G), or late therapeutic mode (H) (original magnification × 50). Reproduced with permission from reference Sugimoto et al[66].