IL-6 stimulates intestinal epithelial proliferation and repair after injury.
IL-6 stimulates intestinal epithelial proliferation and repair after injury.
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DOI：
10.1371/journal.pone.0114195
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Stappenbeck TS
中科院分区：
文献类型：
--
作者：
Kuhn KA;Manieri NA;Liu TC;Stappenbeck TS
IL-6是一种多效性细胞因子，常与炎症有关。抑制这一途径已经成功地治疗了类风湿性关节炎，但抗IL-6治疗的一个不可预见的潜在并发症是肠穿孔。在肠道内，IL-6已被证明在长期炎症期间可以防止上皮细胞凋亡。IL-6在最初的炎性损伤中在肠道中的作用尚不清楚。在这里，我们评估IL-6在炎症损伤开始时的作用。使用两种小鼠肠道损伤模型--活检造成的损伤和细菌触发的结肠炎--我们证明了损伤后不久，包括上皮内淋巴细胞在内的多种细胞类型都会诱导IL-6的产生。抑制IL-6通过抑制上皮细胞增殖导致创面愈合受阻。使用从因外伤性穿孔而接受结肠手术切除的患者获得的肠道组织，我们观察到穿孔区域内可检测到IL-6的细胞，而不是远端部位。我们的数据表明，在炎症损伤开始时，部分由上皮内淋巴细胞产生的IL-6对于上皮细胞增殖和伤口修复具有重要作用。
IL-6 is a pleiotropic cytokine often associated with inflammation. Inhibition of this pathway has led to successful treatment of rheumatoid arthritis, but one unforeseen potential complication of anti-IL-6 therapy is bowel perforation. Within the intestine, IL-6 has been shown to prevent epithelial apoptosis during prolonged inflammation. The role of IL-6 in the intestine during an initial inflammatory insult is unknown. Here, we evaluate the role of IL-6 at the onset of an inflammatory injury. Using two murine models of bowel injury – wound by biopsy and bacterial triggered colitis – we demonstrated that IL-6 is induced soon after injury by multiple cell types including intraepithelial lymphocytes. Inhibition of IL-6 resulted in impaired wound healing due to decreased epithelial proliferation. Using intestinal tissue obtained from patients who underwent surgical resection of the colon due to traumatic perforation, we observed cells with detectable IL-6 within the area of perforation and not at distant sites. Our data demonstrate the important role of IL-6 produced in part by intraepithelial lymphocytes at the onset of an inflammatory injury for epithelial proliferation and wound repair.
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影响因子：
15.8
作者：
Kang, Silvia S.;Bloom, Seth M.;Norian, Lyse A.;Geske, Michael J.;Flavell, Richard A.;Stappenbeck, Thaddeus S.;Allen, Paul M.
通讯作者：
Allen, Paul M.
影响因子：
29.4
作者：
Ito, H;Takazoe, M;Kishimoto, T
通讯作者：
Kishimoto, T
DOI：
10.1073/pnas.0803343106
发表时间：
2009-01-06
影响因子：
11.1
作者：
Seno, Hiroshi;Miyoshi, Hiroyuki;Stappenbeck, Thaddeus S.
通讯作者：
Stappenbeck, Thaddeus S.
影响因子：
9.7
作者：
Schneider, MR;Hoeflich, A;Lahm, H
通讯作者：
Lahm, H
影响因子：
50.3
作者：
Bollrath, Julia;Phesse, Toby J.;Greten, Florian R.
通讯作者：
Greten, Florian R.