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首页> 外文期刊>Cytokine >Continuous interferon-gamma or tumor necrosis factor-alpha exposure of enterocytes attenuates cell death responses.
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Continuous interferon-gamma or tumor necrosis factor-alpha exposure of enterocytes attenuates cell death responses.

机译：连续干扰素-γ或肿瘤坏死因子-α暴露于肠细胞会减弱细胞死亡反应。

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摘要

Short-term stimulation (i.e. <2 days) with tumor necrosis factor-alpha (TNF-alpha) or interferon-gamma (IFN-gamma) cause growth arrest and sensitize epithelial cells to CD95 (Fas/Apo-1)-mediated cell death. The effect of long-term cytokine exposure on viability, proliferation, and apoptosis response of colonic epithelial cells is unknown and addressed in this study. In the present study HT29 and DLD-1 colonic cells were stimulated with either TNF-alpha or IFN-gamma at varying concentrations for 2-9 days. Viability and proliferation was assessed. CD95-mediated cell death response was determined. IFN-gamma caused decreased viability at high concentrations (1nM), whereas lower concentrations (10-100pM) only caused a transient growth arrest. TNF-alpha (100pM) did not affect cell growth. Cells stimulated for 8 days with IFN-gamma (10pM) or TNF-alpha (100pM) had higher proliferation rates than controls or cells stimulated for 2 days ( [Formula: see text] ). Whereas the spontaneous cell death increased slightly during continuous cytokine exposure the CD95L response decreased ( [Formula: see text] ). Colonic cells continuously exposed to IFN-gamma or TNF-alpha had cell turnover characteristics that resemble findings in patients with UC. Increased proliferation and decreased cell death response may act as a counter regulatory mechanism that limits the damaging effects of cytokines.
机译：肿瘤坏死因子-α（TNF-α）或干扰素-γ（IFN-γ）的短期刺激（即<2天）可导致生长停滞并使上皮细胞对CD95（Fas / Apo-1）介导的细胞死亡敏感。长期暴露于细胞因子对结肠上皮细胞的活力，增殖和凋亡反应的影响尚不清楚，并且在本研究中得到了解决。在本研究中，以不同浓度的TNF-α或IFN-γ刺激HT29和DLD-1结肠细胞2-9天。评估生存力和增殖。确定了CD95介导的细胞死亡反应。 IFN-γ导致高浓度（1nM）时活力降低，而较低浓度（10-100pM）仅引起瞬时生长停滞。 TNF-α（100pM）不影响细胞生长。用IFN-γ（10pM）或TNF-alpha（100pM）刺激8天的细胞具有比对照组或刺激2天的细胞更高的增殖率（[公式：参见文本]）。在连续暴露于细胞因子期间，自发细胞死亡略有增加，而CD95L反应则有所降低（[公式：参见正文]）。连续暴露于IFN-γ或TNF-α的结肠细胞具有类似于UC患者的细胞更新特征。增加的增殖和减少的细胞死亡反应可以作为限制细胞因子破坏作用的反调节机制。

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