Document Detail


Elevated maternal IL-16 levels, enhanced IL-16 expressions in endothelium and leukocytes, and increased IL-16 production by placental trophoblasts in women with preeclampsia.
MedLine Citation:
PMID:  18768901     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Yang Gu; David F Lewis; Kelli Deere; Lynn J Groome; Yuping Wang
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  181     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2008 Sep 
Date Detail:
Created Date:  2008-09-04     Completed Date:  2008-11-18     Revised Date:  2014-09-12    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4418-22     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Adult
Endothelium, Vascular / immunology*,  metabolism,  pathology
Female
Humans
Inflammation Mediators / metabolism,  physiology
Interleukin-16 / biosynthesis,  genetics,  metabolism*
Leukocytes / immunology*,  metabolism,  pathology
Organ Culture Techniques
Placenta / cytology,  immunology,  metabolism
Pre-Eclampsia / immunology*,  metabolism,  pathology
Pregnancy
Severity of Illness Index
Trophoblasts / immunology*,  metabolism,  pathology
Up-Regulation / genetics,  immunology*
Grant Support
ID/Acronym/Agency:
HD36822/HD/NICHD NIH HHS; HL65997/HL/NHLBI NIH HHS; R01 HD036822/HD/NICHD NIH HHS; R01 HD036822-08/HD/NICHD NIH HHS; R01 HL065997/HL/NHLBI NIH HHS; R01 HL065997-08/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Interleukin-16
Comments/Corrections

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