Neonatology

Original Paper

Association of Interleukin-13/-4 and Toll-Like Receptor 10 with Preterm Births

Heinzmann A. · Mailaparambil B. · Mingirulli N. · Krueger M.

Author affiliations

Centre for Pediatrics and Adolescent Medicine, University of Freiburg, Freiburg, Germany

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Neonatology 2009;96:175–181

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: August 05, 2008
Accepted: October 10, 2008
Published online: March 31, 2009
Issue release date: September 2009

Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 5

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: https://www.karger.com/NEO

Abstract

Background: Preterm birth (PTB) is accompanied by an increased neonatal morbidity. The cause of PTB is multifactorial and the interplay between environmental and genetic factors – of mothers and newborns – determines the risk. Objectives: We were interested to identify fetal genes predisposing to PTB in the German population. Methods: We started our study by screening 31 polymorphisms within 15 genes of 121 preterm infants born below 32 gestational weeks and 270 healthy controls. Genotyping was performed by restriction fragment length polymorphism. Statistical analyses used Armitage’s trend test for single polymorphisms and FAMHAP for calculation of haplotypes. Results: No single polymorphism showed association with PTB; however, haplotypes of interleukin (IL)-13/IL-4 and Toll-like receptor (TLR)-10 were associated (p = 0.0001 and p = 0.0011, respectively). The association was further confirmed in an extended population of a total of 164 preterm infants. Furthermore, one polymorphism in IL-13 showed a weak association with PTB in this population (p = 0.031). Finally, we analyzed whether the cause of PTB, i.e. medically indicated cesarean section versus spontaneous PTB, affects association results and found evidence in favor of a separate analysis of both groups. Conclusions: IL-13/IL-4 and TLR-10 might be involved in the genetics of PTB. The dissection of the genetic background may provide a deeper understanding of the pathophysiology of PTB and help to identify new drug targets for its prevention.

© 2009 S. Karger AG, Basel




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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: August 05, 2008
Accepted: October 10, 2008
Published online: March 31, 2009
Issue release date: September 2009

Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 5

ISSN: 1661-7800 (Print)
eISSN: 1661-7819 (Online)

For additional information: https://www.karger.com/NEO


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