Differential effects of the CpG-Toll-like receptor 9 axis on pregnancy outcome in nonobese diabetic mice and wild-type controls.
Differential effects of the CpG-Toll-like receptor 9 axis on pregnancy outcome in nonobese diabetic mice and wild-type controls.
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DOI：
10.1016/j.fertnstert.2013.01.121
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发表时间：
2013-05
影响因子：
6.7
通讯作者：
Lin, Yi
中科院分区：
文献类型：
--
作者：
Sun, Yun;Qin, Xiaoli;Shan, Bin;Wang, Wenjing;Zhu, Qinling;Sharma, Surendra;Wu, Ji;Lin, Yi
目的：探讨cpg诱导的先天免疫激活与妊娠结局的关系。一项基于动物模型的研究。学术。将妊娠非肥胖糖尿病小鼠（NOD）与非免疫缺陷小鼠进行比较。我们在怀孕野生型（WT）和自然杀伤型（NK）细胞缺陷NOD小鼠中使用CpG ODN模拟toll样受体9 （TLR9）的激活。妊娠小鼠胎儿吸收和早产的评价流式细胞分析和ELISA检测。cpg诱导的胎儿吸收或早产仅在NOD小鼠中稳定观察到，而在WT小鼠中没有观察到。同时，CpG处理引发子宫巨噬细胞和中性粒细胞的扩增。此外，CpG诱导子宫CD11b+F4/80+细胞产生的血清小鼠角化细胞源性细胞因子（mKC）和肿瘤坏死因子-α (TNF-α)显著增加，而NK和CD11b+Gr-1+细胞则不产生。此外，消耗F4/80+细胞消除了CpG诱导的TNF-α产生的增加，并改善了CpG处理NOD小鼠的妊娠结局。这些结果提供了证据，cpg驱动的先天免疫激活可能导致巨噬细胞的激活和扩增，随后它们迁移到胎母微环境，上调TNF-α的产生，以及随之而来的不良妊娠结局。
To elucidate the relationship between CpG-induced activation of innate immunity and pregnancy outcome. An animal model-based study. Academic. Pregnant nonobese diabetic (NOD) mice were compared with nonimmunodeficient mice. We mimic toll-like receptor 9 (TLR9) activation using CpG ODN administration in pregnant wild-type (WT) and natural killer (NK) cell–deficient NOD mice. Evaluation of fetal resorption and preterm birth in pregnant mice; flow-cytometric analysis and ELISA detection. CpG-induced fetal resorption or preterm birth was observed steadily only in NOD mice but not in WT mice. Concurrently, CpG treatment triggered amplification of uterine macrophages and neutrophils. Moreover, CpG induced a substantial increase of serum mouse keratinocyte-derived cytokine (mKC) and tumor necrosis factor-α (TNF-α) that were produced by uterine CD11b+F4/80+ cells but not by NK or CD11b+Gr-1+ cells. In addition, depletion of F4/80+ cells abrogated a CpG-induced increase in TNF-α production and improved pregnancy outcomes in NOD mice treated with CpG. These results provide evidence that CpG-driven innate immune activation may lead to activation and amplification of macrophages followed by their migration to fetomaternal microenvironment, up-regulated TNF-α production, and consequent adverse pregnancy outcomes.
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DOI：
10.4049/jimmunol.0900788
发表时间：
2009-07-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Thaxton JE;Romero R;Sharma S
通讯作者：
Sharma S
影响因子：
9.8
作者：
Murphy, Shaun P.;Hanna, Nazeeh N.;Fast, Loren D.;Shaw, Sunil K.;Berg, Goeran;Padbury, James F.;Romero, Roberto;Sharma, Surendra
通讯作者：
Sharma, Surendra
影响因子：
4.4
作者：
Gursel, I;Gursel, M;Klinman, DM
通讯作者：
Klinman, DM
TLR3 和 TLR7 激活对非肥胖糖尿病 (NOD) 小鼠子宫 NK 细胞的影响。
影响因子：
3.4
作者：
Lin, Yi;Ren, Lingling;Saito, Shigeru
通讯作者：
Saito, Shigeru
影响因子：
6.7
作者：
Lin, Yi;Xu, Liang;Lin, Qi-de
通讯作者：
Lin, Qi-de