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IL-10 treatment is associated with prohibitin expression in the Crohn's disease intestinal fibrosis mouse model.

Yuan C, Chen WX, Zhu JS, Chen NW, Lu YM, Ou YX, Chen HQ - Mediators Inflamm. (2013)

Bottom Line: Fluorescence-based quantitative polymerase chain reaction (FQ-PCR) and immunohistochemistry assays revealed a significant upregulation of prohibitin with IL-10 treatment.Furthermore, IL-10 decreases inflammatory cytokines and TGF-β1 in the IL-10KO model of Crohn's disease and demonstrates a promising trend in decreasing tissue fibrosis.In conclusion, we hypothesize that IL-10 treatment is associated with increased prohibitin and would decrease inflammation and fibrosis in an animal model of Crohn's disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, China.

ABSTRACT
Prohibitin, which can inhibit oxidative stress and mitochondrial dysfunction, has been shown to have significant anti-inflammatory activities. Here, we investigate the effects of altering prohibitin levels in affected tissues in the interleukin-10 knockout (IL-10KO) mouse model with intestinal fibrosis. The aim of this study is to investigate the effects of IL-10 on prohibitin and the role of prohibitin in intestinal fibrosis of murine colitis. After the mice were treated with IL-10, prohibitin expression and localization were evaluated in IL-10KO and wild-type (WT, 129/SvEv) mice. The colon tissue was then investigated and the potential pathogenic molecular mechanisms were further studied. Fluorescence-based quantitative polymerase chain reaction (FQ-PCR) and immunohistochemistry assays revealed a significant upregulation of prohibitin with IL-10 treatment. Furthermore, IL-10 decreases inflammatory cytokines and TGF-β1 in the IL-10KO model of Crohn's disease and demonstrates a promising trend in decreasing tissue fibrosis. In conclusion, we hypothesize that IL-10 treatment is associated with increased prohibitin and would decrease inflammation and fibrosis in an animal model of Crohn's disease. Interestingly, prohibitin may be a potential target for intestinal fibrosis associated with inflammatory bowel disease (IBD).

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Trichrome image analysis: collagen I in colonic (%) *P < 0.05, versus control group; **P < 0.05, versus IL-10KO mice group.
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fig4: Trichrome image analysis: collagen I in colonic (%) *P < 0.05, versus control group; **P < 0.05, versus IL-10KO mice group.

Mentions: The H&E staining histologic findings revealed colonic epithelial hyperplasia, crypt abscess, glands arranged in disorder, and the forming of edema and ulceration of submucosa in the propria of the colonic tissue from IL-10KO mice at 12, 14, and 16 weeks of age (Figures 2(d)–2(f)). IL-10 treatment led to a significant amelioration of colonic epithelial hyperplasia and cellular infiltration with IL-10 treatment (Figures 2(b) and 2(c)). The histopathological colitis score in the IL-10KO mice group was significantly increased with age and was greater in IL-10KO mice than in the control group at each time point. In treatment group, the histopathological colitis score was decreased significantly than those in IL-10KO mice group at week 16 (Table 1, P < 0.05). Masson's trichrome stain sections of the colon were analyzed for collagen content as described in Section 2 (Figure 4). In WT mice, little collagen deposition was found in the mesenchymal layer. On the other hand, collagen deposition in IL-10KO mice was localized not only in the mesenchymal but also in the mucosa, submucosal, and muscularis propria areas. We then found that collagen deposition was increased with age, specifically at 12-, 14-, and 16-week time points (Figures 3(d)–3(f)). Furthermore, the amount of collagen deposited in the submucosal areas and muscularis propria was markedly reduced in the IL-10-treated group compared to that in the IL-10KO mice (Figures 3(b) and 3(c),  P < 0.05).


IL-10 treatment is associated with prohibitin expression in the Crohn's disease intestinal fibrosis mouse model.

Yuan C, Chen WX, Zhu JS, Chen NW, Lu YM, Ou YX, Chen HQ - Mediators Inflamm. (2013)

Trichrome image analysis: collagen I in colonic (%) *P < 0.05, versus control group; **P < 0.05, versus IL-10KO mice group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3649775&req=5

fig4: Trichrome image analysis: collagen I in colonic (%) *P < 0.05, versus control group; **P < 0.05, versus IL-10KO mice group.
Mentions: The H&E staining histologic findings revealed colonic epithelial hyperplasia, crypt abscess, glands arranged in disorder, and the forming of edema and ulceration of submucosa in the propria of the colonic tissue from IL-10KO mice at 12, 14, and 16 weeks of age (Figures 2(d)–2(f)). IL-10 treatment led to a significant amelioration of colonic epithelial hyperplasia and cellular infiltration with IL-10 treatment (Figures 2(b) and 2(c)). The histopathological colitis score in the IL-10KO mice group was significantly increased with age and was greater in IL-10KO mice than in the control group at each time point. In treatment group, the histopathological colitis score was decreased significantly than those in IL-10KO mice group at week 16 (Table 1, P < 0.05). Masson's trichrome stain sections of the colon were analyzed for collagen content as described in Section 2 (Figure 4). In WT mice, little collagen deposition was found in the mesenchymal layer. On the other hand, collagen deposition in IL-10KO mice was localized not only in the mesenchymal but also in the mucosa, submucosal, and muscularis propria areas. We then found that collagen deposition was increased with age, specifically at 12-, 14-, and 16-week time points (Figures 3(d)–3(f)). Furthermore, the amount of collagen deposited in the submucosal areas and muscularis propria was markedly reduced in the IL-10-treated group compared to that in the IL-10KO mice (Figures 3(b) and 3(c),  P < 0.05).

Bottom Line: Fluorescence-based quantitative polymerase chain reaction (FQ-PCR) and immunohistochemistry assays revealed a significant upregulation of prohibitin with IL-10 treatment.Furthermore, IL-10 decreases inflammatory cytokines and TGF-β1 in the IL-10KO model of Crohn's disease and demonstrates a promising trend in decreasing tissue fibrosis.In conclusion, we hypothesize that IL-10 treatment is associated with increased prohibitin and would decrease inflammation and fibrosis in an animal model of Crohn's disease.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai 200233, China.

ABSTRACT
Prohibitin, which can inhibit oxidative stress and mitochondrial dysfunction, has been shown to have significant anti-inflammatory activities. Here, we investigate the effects of altering prohibitin levels in affected tissues in the interleukin-10 knockout (IL-10KO) mouse model with intestinal fibrosis. The aim of this study is to investigate the effects of IL-10 on prohibitin and the role of prohibitin in intestinal fibrosis of murine colitis. After the mice were treated with IL-10, prohibitin expression and localization were evaluated in IL-10KO and wild-type (WT, 129/SvEv) mice. The colon tissue was then investigated and the potential pathogenic molecular mechanisms were further studied. Fluorescence-based quantitative polymerase chain reaction (FQ-PCR) and immunohistochemistry assays revealed a significant upregulation of prohibitin with IL-10 treatment. Furthermore, IL-10 decreases inflammatory cytokines and TGF-β1 in the IL-10KO model of Crohn's disease and demonstrates a promising trend in decreasing tissue fibrosis. In conclusion, we hypothesize that IL-10 treatment is associated with increased prohibitin and would decrease inflammation and fibrosis in an animal model of Crohn's disease. Interestingly, prohibitin may be a potential target for intestinal fibrosis associated with inflammatory bowel disease (IBD).

Show MeSH
Related in: MedlinePlus