Paracrine mediators of mouse uterine epithelial cell transepithelial resistance in culture

Paracrine mediators of mouse uterine epithelial cell transepithelial resistance in culture
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DOI:
10.1016/j.jri.2005.06.001
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发表时间:
2005-10-01
影响因子:
3.4
通讯作者:
Wira, CR
Wira, CR
中科院分区:
医学4区
文献类型:
--
作者:
Grant-Tschudy, KS;Wira, CR

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粘膜表面上皮细胞的完整性为抵抗潜在的威胁生殖健康的病原体提供了有效的物理屏障。我们利用成年小鼠子宫极化上皮细胞,研究了子宫上皮细胞和间质细胞产生的TNF α和TGF β,以及子宫间质细胞产生的肝细胞生长因子(HGF)在调节上皮细胞完整性(经上皮电阻(TER)测量)中的作用。上皮细胞暴露于TNF - α、TGF - β和HGF对TER的深远影响不同于它们对其他粘膜表面TER的已知作用。当与TNF α孵育时,TER呈剂量依赖性增加。相反,当细胞与TGF β孵育时,TER明显但可逆地受到抑制。有趣的是,当HGF放置在基底外侧腔室时,增加了TER。基于这些发现,我们认为TNF α、TGF β和HGF可能在调节上皮细胞紧密连接中发挥调节作用。这些研究表明,激素平衡、病原体暴露和妊娠等影响细胞因子和生长因子分泌的因素影响了女性生殖道上皮细胞屏障的保护。2005爱思唯尔爱尔兰有限公司版权所有。
Epithelial cell integrity at mucosal surfaces provides an effective physical barrier against potential pathogens that threaten reproductive health. We have used polarized epithelial cells from adult mouse uteri to investigate the roles of TNF alpha and TGF beta, which are produced by uterine epithelial and stromal cells, and hepatocyte growth factor (HGF), produced by uterine stromal cells, in regulating epithelial cell integrity measured as transepithelial electrical resistance (TER). Exposure of epithelial cells to TNF alpha, TGF beta, and HGF have profound effects on TER that are different from their known actions on TER at other mucosal surfaces. When incubated with TNF alpha, TER increased in a dose-dependent manner. In contrast, when cells were incubated with TGF beta, TER was markedly but reversibly suppressed. Interestingly, HGF, when placed in the basolateral compartment, increased TER. Based on these findings, we conclude that TNF alpha, TGF beta and HGF may play regulatory roles in modulating epithelial cell tight junctions. These studies suggest that factors, such as hormone balance, pathogen exposure as well as pregnancy, which affect cytokine and growth factor secretion, influence epithelial cell barrier protection within the female reproductive tract. (c) 2005 Elsevier Ireland Ltd. All rights reserved.