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Maternal lipopolysaccharide alters the newborn oxidative stress and C-reactive protein levels in response to an inflammatory stress

Published online by Cambridge University Press:  25 April 2012

Y. Ginsberg ,
P. Lotan ,
N. Khatib ,
N. Awad ,
S. Errison ,
Z. Weiner ,
N. Maravi ,
M. G. Ross ,
J. Itskovitz-Eldor  and
R. Beloosesky
Y. Ginsberg
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
P. Lotan
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
N. Khatib
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
N. Awad
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
S. Errison
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
Z. Weiner
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
N. Maravi
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
M. G. Ross
Affiliation:
Department of Obstetrics and Gynecology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA
J. Itskovitz-Eldor
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel
R. Beloosesky*
Affiliation:
Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel Department of Obstetrics and Gynecology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA
*
*Address for correspondence: Dr R. Beloosesky, Department of Obstetrics and Gynecology, Rambam Medical Center, Haifa, Israel. Email [email protected]
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Abstract

Maternal infection is associated with oxidative stress (OS) and inflammatory responses. We have previously shown that maternal exposure to lipopolysaccharide (LPS) at E18 alters the subsequent offspring immune response. As immune responses are mediated, in part, by OS, we sought to determine if maternal inflammation during pregnancy programs offspring OS and C-reactive protein (CRP) levels. Pregnant Sprague-Dawley rats received intraperitoneal (i.p.) injections of saline or LPS at 18 days’ gestation (n = 4), and pups delivered spontaneously at term. At postnatal day 24, male and female offspring received i.p. injection of LPS. Serum lipid peroxides formation (PD) and CRP levels were determined before and at 4 h following the LPS injection. Pups of LPS-exposed dams had significantly higher basal OS (PD 29.4 ± 5.4 v. 10.1 ± 4.8 nmol/ml) compared with controls. In response to LPS, CRP levels (20.4 ± 2.8 v. 5.7 ± 1.0 ng/ml) were significantly higher among pups of LPS-exposed dams than controls. Prenatal maternal exposure to LPS increases baseline OS levels in neonates and CRP levels in response to LPS. These results suggest that maternal inflammation during the antenatal period may induce long-term sequelae in the offspring that may predispose to adult disease.

Keywords

inflammationnewbornoxidative stresspregnancy
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 3 , Issue 5 , October 2012 , pp. 358 - 363
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2012

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