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Elevated Maternal IL-16 Levels, Enhanced IL-16 Expressions in Endothelium and Leukocytes, and Increased IL-16 Production by Placental Trophoblasts in Women with Preeclampsia¹

Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, Shreveport, LA 71130

Cytokine IL-16 plays an important role in innate immune responses. However, little information is available about IL-16 function in human pregnancy. In this study, we collected maternal blood samples from 125 pregnant women between 26 and 41 wk of gestation, 63 from normal pregnant women and 62 from women with preeclampsia (PE). Serum IL-16C levels were measured by ELISA. We also examined IL-16C and IL-16N immunostaining in maternal vessels and protein expression in leukocytes from normal and PE pregnant women. In addition, IL-16C production by placental trophoblasts was also determined. Our results showed that IL-16C levels were significantly higher in severe PE than in mild PE and normal pregnant controls, 515 ± 58 vs 287 ± 46 (p < 0.05) and 163 ± 9 pg/ml (p < 0.01), respectively, indicating that increased IL-16 levels in PE is associated with the severity of the disease. There was no difference for the IL-16C levels in normal pregnant women throughout the third trimester. The correlation of maternal IL-16C levels with labor and body mass index was also analyzed. IL-16C levels were neither associated with labor nor associated with body mass index. Moreover, increased IL-16C immunostaining in maternal vessel endothelium and enhanced IL-16C protein expression in leukocytes were observed in PE. We also found that IL-16C production was increased by trophoblasts from PE placentas. Our study demonstrated up-regulation of the IL-16 profile in both the maternal and the placental systems in PE, suggesting that IL-16 could be an important cytokine engaged in the altered immune system and exaggerated inflammatory response in PE syndrome.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by grants from National Institute of Health, National Heart, Lung, and Blood Institute (HL65997), and National Institute of Child Health and Human Development (HD36822).

² Address correspondence and reprint requests to Dr. Yuping Wang, Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center-Shreveport, PO Box 33932, Shreveport, LA 71130. E-mail address: ywang1{at}lsuhsc.edu

³ Abbreviations used in this paper: PE, preeclampsia; BMI, body mass index.