2. Academic Validation
  3. Placenta-derived IL-32β activates neutrophils to promote preeclampsia development

Placenta-derived IL-32β activates neutrophils to promote preeclampsia development

  • Cell Mol Immunol. 2021 Apr;18(4):979-991. doi: 10.1038/s41423-021-00636-5.
Dan Liu 1,  Qiang Li 2,  Hailin Ding 1,  Guangfeng Zhao 1,  Zhiyin Wang 1,  Chenrui Cao 1,  Yimin Dai 1,  Mingming Zheng 1,  Xiangyu Zhu 1,  Qianwen Wu 1,  Ya Wang 1,  Honglei Duan 1,  Huirong Tang 1,  Xianyan Lu 1,  Yayi Hou 3,  Yali Hu 4 5
Affiliations

Affiliations

  • 1 Department of Obstetrics and Gynecology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China.
  • 2 Department of Obstetrics and Gynecology, Drum Tower Clinic Medical College of Nanjing Medical University, Nanjing, Jiangsu, China.
  • 3 The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, China. yayihou@nju.edu.cn.
  • 4 Department of Obstetrics and Gynecology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, China. yalihu@nju.edu.cn.
  • 5 Department of Obstetrics and Gynecology, Drum Tower Clinic Medical College of Nanjing Medical University, Nanjing, Jiangsu, China. yalihu@nju.edu.cn.
PMID: 33707686 DOI: 10.1038/s41423-021-00636-5
Abstract

Immune activation at the maternal-fetal interface is a main pathogenic factor of preeclampsia (PE). Neutrophils (PMNs) are activated in PE patients, but the mechanism and consequences of PMN activation need to be further explored. Here, we demonstrated that interleukin-32 (IL-32) expression was significantly upregulated in syncytiotrophoblasts (STBs) and that IL-32β was the major isoform with increased expression in the placenta of severe PE (sPE) patients. Furthermore, the level of IL-32 expression in the placenta was correlated with its level in the serum of sPE patients, indicating that IL-32 in the serum is derived mainly from the placenta. Then, in vitro experiments showed that IL-32β could highly activate PMNs and that these IL-32β-activated PMNs were better able to adhere to endothelial cells (HUVECs) and enhance the expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) in HUVECs, which could be reversed by preincubation with the NADPH Oxidase Inhibitor VAS 2870. In addition, we showed that IL-32β mainly activated PMNs by binding to proteinase 3. Finally, IL-32β administration induced a PE-like phenotype in a pregnant mouse model. This study provides evidence of the involvement of IL-32β in the pathogenesis of PE.

Keywords

HUVEC; IL-32; Neutrophil; Preeclampsia; ROS.

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