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炎症性肠病治疗与结肠炎小鼠模型中的肠道功能

Inflammatory bowel disease therapies and gut function in a colitis mouse model.

机构信息

School of Women's and Children's Health, University of New South Wales, Randwick, Sydney, NSW 2031, Australia.

出版信息

Biomed Res Int. 2013;2013:909613. doi: 10.1155/2013/909613. Epub 2013 Aug 6.

DOI:10.1155/2013/909613
PMID:24027765
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3763566/
Abstract

BACKGROUND

Exclusive enteral nutrition (EEN) is a well-established approach to the management of Crohn's disease. Aim. To determine effects of EEN upon inflammation and gut barrier function in a colitis mouse model.

METHODS

Interleukin-10-deficient mice (IL-10(-/-)) were inoculated with Helicobacter trogontum and then treated with EEN, metronidazole, hydrocortisone, or EEN and metronidazole combination. Blood and tissue were collected at 2 and 4 weeks with histology, mucosal integrity, tight junction integrity, inflammation, and H. trogontum load evaluated.

RESULTS

H. trogontum induced colitis in IL-10(-/-) mice with histological changes in the cecum and colon. Elevated mucosal IL-8 mRNA in infected mice was associated with intestinal barrier dysfunction indicated by decreased transepithelial electrical resistance and mRNA of tight junction proteins and increased short-circuit current, myosin light chain kinase mRNA, paracellular permeability, and tumor necrosis factor- α and myeloperoxidase plasma levels (P < 0.01 for all comparisons). EEN and metronidazole, but not hydrocortisone, treatments restored barrier function, maintained gut barrier integrity, and reversed inflammatory changes along with reduction of H. trogontum load (versus infected controls P < 0.05).

CONCLUSION

H. trogontum infection in IL-10(-/-) mice induced typhlocolitis with intestinal barrier dysfunction. EEN and metronidazole, but not hydrocortisone, modulate barrier dysfunction and reversal of inflammatory changes.

摘要

背景

肠内营养（EEN）是一种成熟的克罗恩病管理方法。目的。在结肠炎小鼠模型中确定 EEN 对炎症和肠道屏障功能的影响。

方法

将白细胞介素-10 缺陷型（IL-10(-/-)）小鼠接种幽门螺杆菌，然后用 EEN、甲硝唑、氢化可的松或 EEN 和甲硝唑联合治疗。在第 2 周和第 4 周收集血液和组织，评估组织学、黏膜完整性、紧密连接完整性、炎症和 H. trogontum 负荷。

结果

H. trogontum 在 IL-10(-/-) 小鼠中诱导结肠炎，回肠和结肠有组织学变化。感染小鼠的黏膜 IL-8 mRNA 升高与肠道屏障功能障碍相关，表现为跨上皮电阻降低，紧密连接蛋白的 mRNA 减少，短circuit 电流增加，肌球蛋白轻链激酶 mRNA、细胞旁通透性增加，肿瘤坏死因子-α和髓过氧化物酶血浆水平升高（所有比较均为 P < 0.01）。EEN 和甲硝唑治疗，而不是氢化可的松治疗，恢复了屏障功能，维持了肠道屏障完整性，并逆转了炎症变化，同时降低了 H. trogontum 负荷（与感染对照组相比 P < 0.05）。

结论

IL-10(-/-) 小鼠中的 H. trogontum 感染引起回结肠结肠炎和肠道屏障功能障碍。EEN 和甲硝唑，而不是氢化可的松，可调节屏障功能障碍和炎症变化的逆转。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/4edca46a7041/BMRI2013-909613.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/0cdb01e4a1d7/BMRI2013-909613.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/ac449c5612bf/BMRI2013-909613.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/f45a8505cb87/BMRI2013-909613.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/6ead9444d5ae/BMRI2013-909613.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/9bdaa2abd4d2/BMRI2013-909613.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/9898fb3701eb/BMRI2013-909613.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/4edca46a7041/BMRI2013-909613.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/0cdb01e4a1d7/BMRI2013-909613.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/ac449c5612bf/BMRI2013-909613.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/f45a8505cb87/BMRI2013-909613.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/6ead9444d5ae/BMRI2013-909613.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/9bdaa2abd4d2/BMRI2013-909613.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/9898fb3701eb/BMRI2013-909613.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3137/3763566/4edca46a7041/BMRI2013-909613.007.jpg

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