Neutrophil count is a useful marker to predict the severity of preeclampsia.

BACKGROUND: At present, pre-eclampsia is a growing concern and still a diagnostic challenge for obstetricians. AIMS: This study aimed to evaluate whether the relationship of second trimester of pregnancy neutrophil count differed among pregnancies with mild preeclampsia, severe preeclampsia, and healthy status and explore whether or not neutrophil count in the second trimester of pregnancy would be useful as new predictors of subsequent preeclampsia. PATIENTS AND METHODS: This study involved 933 pregnancies from 1 January 2018 to 30 January 2021, comprising 396 healthy pregnancies, 222 pregnancies with mild preeclampsia, and 315 pregnancies with severe preeclampsia. The relationship between preeclampsia and neutrophil count was analyzed by multiple logistic regression. In addition, maternal placental tissues of three groups were immunohistochemically stained for myeloperoxidase (MPO). RESULTS: Neutrophil count was significantly higher in pregnancies with preeclampsia (including pregnancies with mild and severe preeclampsia) than that in healthy pregnancies. The neutrophil count level was prominently higher in patients with severe preeclampsia compared with those with mild preeclampsia (p < .001). The neutrophil count level was significantly positively associated with preeclampsia after adjusting for gestational week at time of blood sampling, BMI, and age (ß:1.23; 95%CI:1.09-1.36; p < .0001). In addition, MPO expressions of placental tissues in preeclamptic groups were significantly increased than these in healthy pregnant controls (p < .05). CONCLUSIONS: Increased neutrophil count in the second trimester of pregnancy was significantly positively associated with preeclampsia. Hence, neutrophil count plays a role in predicting the severity of preeclampsia. At the same time, it may be an independent predictor of subsequent preeclampsia.Abbreviations: BMI: body mass index; MPO: myeloperoxidase.

Highly expressed FYN promotes the progression of placenta accreta by activating STAT3, p38, and JNK signaling pathways.

Placenta accreta is an abnormality of the placenta caused by the chorionic villi invading the muscular layer, which can cause serious bleeding, infection, shock, bladder invasion, uterine perforation, and even death. However, the etiology of placental accreta is not entirely clear. In the present study, high-throughput sequencing results showed that FYN is highly expressed in the placental accreta position in the placenta accreta group and is a key regulator of cell invasion and migration. Therefore, we aimed to evaluate the role and potential molecular mechanism of FYN in placenta accreta. The results showed that FYN was highly expressed in the placenta tissues of the placenta accreta group. Furthermore, the levels of phosphorylated STAT3, p38, and JNK in the placenta accreta group were remarkably increased compared with those in the control group. In addition, FYN knockdown considerably decreased the migration and invasion rates of trophoblast cells (HTR8/SVneo) and inhibited the levels of phosphorylated STAT3, p38, and JNK. After subsequently blocking these signaling pathways, the invasion and migration abilities of HTR8/SVneo cells were substantially decreased. In conclusion, FYN may promote excessive trophocyte cell invasion by activating STAT3, p38, and JNK pathways and can be a new target for placenta accreta prevention and treatment.