依赖 CCR2 的炎性单核细胞胎盘迁移可抑制弓形虫感染引起的异常妊娠。

IF 4.8 4区 医学 Q2 IMMUNOLOGY
Naganori Kamiyama, Mai Ueno, Yuma Sasaki, Thanyakorn Chalalai, Nozomi Sachi, Sotaro Ozaka, Yasuhiro Soga, Yomei Kagoshima, Supanuch Ekronarongchai, Masaaki Okamoto, Masahiro Yamamoto, Takashi Kobayashi
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引用次数: 0

摘要

弓形虫(T. gongii)是一种人畜共患病原生寄生虫,可导致先天性弓形虫病,包括胎儿死亡、流产、死胎、形态异常和早产。孕妇原发性弓形虫感染会导致先天性弓形虫病。据报道,C-C 趋化因子受体(CCR)2 是宿主抵抗淋球菌感染的关键防御因子。然而,CCR2在先天性弓形虫病中宿主对弓形虫的免疫反应中所起作用的细节仍不清楚。在这里,我们用刚地弓形虫感染了CCR2缺陷的怀孕小鼠,结果小鼠死胎、胚胎再吸收、胎儿形态异常和早产的发生率明显高于野生型怀孕小鼠。与异常妊娠的严重程度一致,在CCR2缺陷小鼠的胎盘中观察到大面积的胎盘出血和出血区周围大量的淋球菌感染。此外,在感染过程中,CCR2缺陷小鼠胎盘中炎性单核细胞的聚集也有所减少。我们进一步证实,将从野生型小鼠体内收集的炎性单核细胞收养转移到感染了淋球菌的 CCR2 缺失型妊娠小鼠体内,能有效抑制胎盘损伤和异常妊娠。总之,CCR2通过调节炎性单核细胞迁移到感染了淋病的怀孕小鼠胎盘中来维持妊娠。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CCR2-dependent placental migration of inflammatory monocytes suppresses abnormal pregnancies caused by Toxoplasma gondii infection.

Toxoplasma gondii (T. gongii) is a zoonotic protozoan parasite that causes congenital toxoplasmosis, including fetal death, abortion, stillbirth, morphological abnormalities, and premature birth. Primary T. gondii infection in pregnant women results in congenital toxoplasmosis. C-C chemokine receptor (CCR) 2 is reportedly a critical host defense factor against T. gondii infection. However, details of the role of CCR2 in the host immune response to T. gondii in congenital toxoplasmosis remain unclear. Here, we infected pregnant CCR2-deficient mice with T. gondii, resulting in stillbirth, embryonic resorption, fetal morphological abnormalities, and preterm delivery at significantly higher rates than those in pregnant wild-type mice. Consistent with the severity of abnormal pregnancy, a large area of placental hemorrhage and a large number of T. gondii infections around the hemorrhagic area were observed in the placentas of CCR2-deficient mice. In addition, the accumulation of inflammatory monocytes in the placenta was reduced in CCR2-deficient mice during infection. We further confirmed that the adoptive transfer of inflammatory monocytes collected from wild-type mice into T. gondii-infected pregnant CCR2-deficient mice effectively suppressed placental damage and abnormal pregnancy. Collectively, CCR2 contributes to pregnancy maintenance by regulating the migration of inflammatory monocytes into the placenta of T. gondii-infected pregnant mice.

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来源期刊
International immunology
International immunology 医学-免疫学
CiteScore
9.30
自引率
2.30%
发文量
51
审稿时长
6-12 weeks
期刊介绍: International Immunology is an online only (from Jan 2018) journal that publishes basic research and clinical studies from all areas of immunology and includes research conducted in laboratories throughout the world.
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