Overexpression of lipocalin 2 in PBX1-deficient decidual NK cells promotes inflammation at the maternal-fetal interface

PBX1 缺陷型蜕膜 NK 细胞中脂质运载蛋白 2 的过度表达会促进母胎界面的炎症

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作者:Xue An, Jingkun Qin, Xinyu Hu, Yonggang Zhou, Binqing Fu, Haiming Wei

Conclusion

Excessive LCN2 secreted by PBX1- dNK cells at the maternal-fetal interface recruit neutrophils and causes an inflammatory response, which is related to FGR.

Results

We verified the embryonic dysplasia in pregnant Pbx1f/f ; Ncr1Cre mice by Doppler ultrasound imaging and found that LCN2 was upregulated in dNK cells. We also observed higher infiltration of neutrophils and macrophages in the decidua of Pbx1f/f ; Ncr1Cre mice. Finally, we found an increase in the number and activation of neutrophils at the maternal-fetal interface after injecting LCN2 into pregnant mice and observed that these mice showed signs of FGR.

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