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首页> 外文学位 >Modulation of interferon-gamma receptor expression during infection with Chlamydia psittaci 6BC and its influence on indoleamine 2,3-dioxygenase.
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Modulation of interferon-gamma receptor expression during infection with Chlamydia psittaci 6BC and its influence on indoleamine 2,3-dioxygenase.

机译：感染鹦鹉热衣原体6BC期间干扰素-γ受体表达的调节及其对吲哚胺2,3-双加氧酶的影响。

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摘要

Interferon-gamma (IFNgamma) induces indoleamine dioxygenase (IDO), which effectively inhibits the growth of intracellular Chlamydia in vitro. Furthermore, tumor necrosis factor-alpha (TNFalpha) and interleukin-1 (IL-1) synergistically increase IFN-induced, anti-chlamydial IDO activity. The mechanism of synergistic IDO activity is multifactorial. While one mechanism is the nuclear factor-kappaB (NF-kappaB)-dependent increase in interferon regulatory factor-1 (IRF-1) activation, increased expression of IFNgamma receptors (IFNgammaR), could also enhance IDO activation. It was found that IFNgammaR expression was up-regulated in epithelial cells upon stimulation with IL-1, also through the transactivation of NF-kappaB. This increase in receptor expression was shown to enhance IDO activity by increasing activation of the transcription factor signal transducer and activator of transcription-1 (STAT-1). Moreover, Chlamydia was found to significantly increase IFNgammaR expression in HeLa cells, even when inactivated, suggesting that chlamydial antigens and not infection up-regulate cytokine receptor expression. Cytokine receptor increase was found to be independent of cytokine secretion as supernatants from infected cells failed to increase IFNgammaR expression. The component of Chlamydia responsible for stimulating the cell to up-regulate cytokine receptor expression is heat stable; receptors increased occurred upon stimulation with Chlamydia inactivated at 100°C. The mechanism by which Chlamydia increases receptor expression requires stimulation of the Toll-like receptors (TLR). While cells either TLR2 or TLR4+MD2 increased IFNgamma receptor expression, cells not possessing TLRs were unresponsive. Similar to IL-1, Chlamydia required TLR-mediated NF-kappaB activation to enhance IFNgammaR expression. However, unlike stimulation with cytokine, no increase in IDO induction was observed. This effect is not due to the inability of IFNgamma to bind to the newly expressed receptors, but rather the impairment in signaling of these receptors. No increase in phosphorylated STAT-1 could be detected in infected cells suggesting that the JAK/STAT pathway was affected.
机译：干扰素-γ（IFNγ）诱导吲哚胺双加氧酶（IDO），在体外有效抑制细胞内衣原体的生长。此外，肿瘤坏死因子-α（TNFalpha）和白介素-1（IL-1）协同增加IFN诱导的抗衣原体IDO活性。 IDO协同作用的机制是多因素的。虽然一种机制是干扰素调节因子1（IRF-1）活化的核因子-κB（NF-kappaB）依赖性增加，但IFNgamma受体（IFNgammaR）的表达增加也可以增强IDO活化。发现通过IL-1刺激，上皮细胞中的IFNgammaR表达也被上调，也通过NF-κB的反式激活。受体表达的这种增加通过增加转录因子信号转导子和转录激活子1（STAT-1）的激活而增强了IDO活性。而且，发现衣原体即使在失活时也能显着增加HeLa细胞中IFNgammaR的表达，这表明衣原体抗原而不是感染会上调细胞因子受体的表达。发现细胞因子受体的增加与细胞因子的分泌无关，因为感染细胞的上清液不能增加IFNgammaR表达。衣原体负责刺激细胞上调细胞因子受体表达的成分是热稳定的。衣原体在100°C失活刺激后，受体增加。衣原体增加受体表达的机制需要刺激Toll样受体（TLR）。虽然TLR2或TLR4 + MD2的细胞会增加IFNγ受体的表达，但不具有TLR的细胞却无反应。与IL-1相似，衣原体需要TLR介导的NF-κB活化才能增强IFNgammaR的表达。然而，与用细胞因子刺激不同，未观察到IDO诱导的增加。该作用不是由于IFNγ不能与新表达的受体结合，而是由于这些受体的信号传导受损。在受感染的细胞中未检测到磷酸化STAT-1的增加，表明JAK / STAT途径受到影响。

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  • 作者

    Shirey, Kari Ann.;

  • 作者单位

    Miami University.;

  • 授予单位 Miami University.;
  • 学科 Biology Microbiology.; Health Sciences Immunology.; Chemistry Biochemistry.
  • 学位 Ph.D.
  • 年度 2006
  • 页码 185 p.
  • 总页数 185
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 微生物学;预防医学、卫生学;生物化学;
  • 关键词

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