目的 探究孕鼠胎盘中性粒细胞和炎性因子白细胞介素17（IL-17）在孕期刚地弓形虫（简称弓形虫）感染致不良妊娠结局中的作用机制。方法 将C57BL/6孕鼠随机分为未感染组和感染组（每组6只)，感染组孕鼠在孕8 d腹腔注射0.2 ml弓形虫RH株速殖子悬液（约400个速殖子），未感染组孕鼠腹腔注射等量灭菌PBS。于孕14 d采用颈椎脱臼法处死孕鼠，解剖观察并记录妊娠结局。取胎盘组织，制备石蜡切片，经苏木苏-伊红（HE）染色后观察胎盘组织学改变和多形核粒细胞的浸润情况，并计算浸润指数。制备胎盘组织单细胞悬液，采用流式细胞术检测胎盘免疫细胞中中性粒细胞。采用免疫组织化学染色检测胎盘组织中弓形虫的分布、定位及IL-17的表达水平（灰度值），采用Spearman相关性分析方法分析IL-17的表达水平与中性粒细胞浸润指数的关系。两组间数据比较采用独立样本Student’s t检验。结果 感染组孕鼠出现弓背、耸毛和行动迟缓等症状，胎鼠和胎盘出现明显出血及淤血点，胎鼠发育不良；未感染组孕鼠无异常表现，胎鼠和胎盘发育正常。感染组孕鼠的流产率为82.35%（42/51），高于未感染组的4.08%（2/49）。HE染色结果显示，感染组孕鼠胎盘组织细胞轮廓性增强，并伴有大量的多形核粒细胞浸润，浸润指数为14.500 ± 0.965，高于未感染组的3.917 ± 0.633（t = 9.168，P < 0.01）。流式细胞术结果显示，感染组孕鼠胎盘组织中中性粒细胞占胎盘细胞的绝对百分数为（13.700±1.790）%，高于未感染组孕鼠的（4.783 ± 0.723）%（t = 5.107，P < 0.01）。免疫组织化学染色结果显示，感染组孕鼠胎盘组织中检测到大量弓形虫，并且主要集中分布于中性粒细胞内；感染组孕鼠胎盘组织中IL-17的灰度值为17.510 ± 1.372，高于未感染组孕鼠的8.178 ± 1.293（t = 4.951，P < 0.05）。相关性分析结果显示，孕鼠胎盘组织中IL-17的表达水平与中性粒细胞的浸润指数呈正相关（R² = 0.652，P < 0.01）。结论 刚地弓形虫感染可导致孕鼠胎盘组织出现大量中性粒细胞浸润和高水平IL-17的表达，IL-17表达水平的升高可能与中性粒细胞在母胎界面的募集有关。

Objective To explore the mechanism of placental neutrophils and IL-17 in adverse pregnancy outcomes of pregnant mice infected with Toxoplasma gondii. Methods C57BL/6 pregnant mice were randomly divided into uninfected group and infected group. Each mouse in the infected group was intraperitoneally injected with 0.2 ml suspension of T. gondii RH strain (about 400 tachyzoites per mouse) on day 8 of gestation. The mice in the uninfected group were intraperitoneally injected with the same amount of sterilized PBS on day 8 of gestation. On day 14 of gestation, the two groups of mice were euthanized by cervical vertebra dislocation to inspect by dissection and record the pregnancy outcome. The placental tissue were sampled to prepare paraffin sections for observing histological changes and infiltration of polymorphonuclear grannulocyes by hematein-eosin (HE) staining to calculate the infiltration index. Additional placental tissues were collected to prepare single-cell suspension, with which the percentages of neutrophils in the placental immune cells were detected by flow cytometry. Immunohistochemical staining was used to detect the distribution and localization of T. gondii and IL-17 expression level (gray value). Spearman correlation analysis was used to analyze the relationship between the IL-17 expression and neutrophil infiltration index. Data between two groups were compared using independent sample Student’s t-test. Results Compared with the uninfected group, the infected group showed significant bleeding and congestion in fetal mice and placenta, fetal dysplasia. The abortion rate in the infected group was 82.35% (42/51), which was higher than that in the uninfected group 4.08% (2/49) (t = 7.683, P < 0.01). HE staining showed that the placental tissue of pregnant mice infected with T. gondii had enhanced hepatocellular contour and was accompanied by a large number of polymorphonuclear granulocytic infiltration. The infiltration index was 14.500 ± 0.965, which was significantly higher than that of the uninfected group (3.917 ± 0.633) (t = 9.168, P < 0.01). Flow cytometryanalysis showed that the percentage of neutrophils in placental cells in the infected group was (13.700 ± 1.790)%, which was significantly higher than that in the uninfected group (4.783 ± 0.723)% (t = 5.107, P < 0.01). Immunohistochemical staining analysis showed that a large number of T. gondii could be detected in the placental tissue and mainly concentrated in neutrophils. The IL-17 intensity in the placenta tissue of the infected pregnant mice (17.510 ± 1.372) was significantly higher than that of uninfected pregnant mice (8.178 ± 1.293) (t = 4.951, P < 0.05). Correlation analysis showed that the expression level of IL-17 in the placenta was positively correlated with the degree of neutrophil infiltration (R² = 0.652, P < 0.01). Conclusion T. gondii infection can lead to a significant infiltration of large number of neutrophils and a high level of IL-17 expression in the placenta tisseus of pregnant mice. The elevated expression level of IL-17 may relate to the recruitment of neutrophils at the maternal-fetal interface.