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首页> 外文期刊>Journal of Cellular Physiology >Transforming growth factor-beta1 preserves epithelial barrier function: identification of receptors, biochemical intermediates, and cytokine antagonists.
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Transforming growth factor-beta1 preserves epithelial barrier function: identification of receptors, biochemical intermediates, and cytokine antagonists.

机译：改变增长factor-beta1保存上皮屏障功能:识别受体、生化中间体细胞因子拮抗剂。

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摘要

Freshly isolated human mucosal T lymphocytes in vitro can markedly diminish an important property of intestinal epithelium-its barrier function. On the other hand, cytokines and their cellular receptors, which maintain homeostasis of epithelia, limit epithelial permeability, and preserve barrier function, are not well characterized. Using a described human colonic epithelial cell monolayer system, we found that transforming growth factor-beta1 (TGF-beta1) preserved 75% or more of epithelial barrier function, quantitated electrophysiologically, even in the presence of cytokines generated by a high density of barrier-disruptive mucosa-derived mononuclear cells. In opposing the TGF-beta1 effect, cytokines able to reduce barrier function were spontaneously secreted by mucosal T cells and were increased in their barrier effect after T-lymphocyte activation. Further, neutralization of individual cytokines with specific monoclonal antibodies abrogated the lymphocyte-induced reduction in epithelial barrier function, and identified interferon gamma (IFN-gamma), interleukin (IL)-4, and IL-10, but not IL-6, as the primary cytokines whose barrier effects were curtailed by TGF-beta1. Receptors (RI and RII) for TGF-beta1 were found to be localized primarily to the apical and basal membranes of surface epithelium in colonic crypts. These findings provide the scientific basis for new strategies to pharmacologically enhance the barrier function of epithelia in mucosal organs regularly exposed to environmental antigens and to T-lymphocyte products. Copyright 1999 Wiley-Liss, Inc.
机译：刚独立的人体粘膜T淋巴细胞体外能显著降低的一个重要属性肠道epithelium-its屏障功能。另一方面,细胞因子和细胞受体,维持体内平衡上皮细胞、上皮通透性限制保护屏障功能,并不好为特征。上皮细胞单层系统,我们发现改变增长factor-beta1 (TGF-beta1)保存75%或更多的上皮屏障函数,量化电生理学,即使在细胞因子产生的存在高密度的barrier-disruptive mucosa-derived单核细胞。功能作用,细胞因子能够减少障碍被粘膜T细胞自发分泌和增加他们的屏障作用早期激活。个人与特定的单克隆细胞因子抗体废除了lymphocyte-induced减少上皮屏障功能,确定干扰素γ(IFN-gamma),白介素4 (IL)和IL - 10,但不是IL - 6,屏障的主要细胞因子的影响由TGF-beta1缩减。为TGF-beta1被发现是本地化主要的顶端和基底膜在结肠隐窝上皮表面。发现提供了新的科学依据从药理学上提高策略在粘膜上皮细胞器官的屏障功能经常暴露于环境抗原和早期的产品。Wiley-Liss公司。

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