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,*
* Mothers and Babies Research Centre and
Respiratory and Sleep Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia;
Department of Psychology, University of Newcastle and
Department of Paediatrics and Reproductive Health, Faculty of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia
In the presence of maternal asthma, we have previously reported reduced placental blood flow, decreased cortisol metabolism, and reductions in fetal growth in response to maternal asthma and asthma exacerbations. We have proposed that these changes in placental function and fetal development may be related to activation of proinflammatory pathways in the placenta in response to maternal asthma. In the present study, we examined the influence of maternal asthma severity, inhaled glucocorticoid treatment, maternal cigarette use, placental macrophage numbers, and fetal sex on placental cytokine mRNA expression from a prospective cohort study of pregnant women with and without asthma. Placental expression of TNF-
, IL-1β, IL-6, IL-8, and IL-5 mRNA were all increased significantly in placentae of female fetuses whose mothers had mild asthma, but no changes were observed in placentae of male fetuses. The proinflammatory cytokines TNF-, IL-1β, and IL-6 were negatively correlated with female cord blood cortisol, but there were no such correlations in placentae from males. Multivariate analysis indicated the strongest predictor of both cytokine mRNA expression in the placenta and birth weight was fetal cortisol but only in females. Placental cytokine mRNA levels were not significantly altered by inhaled glucocorticoid use, placental macrophage numbers, cigarette use, moderate-severe asthma, or male sex. These data suggest that placental basal cytokine mRNA expression is sex specifically regulated in pregnancies complicated by asthma, and interestingly these changes are more prevalent in mild rather than severe asthma.
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 supported by National Health and Medical Research Council (ID 252438), Asthma Foundation of New South Wales, Hunter Medical Research Institute, New South Wales Health. N.S. and A.O.-K. were both awarded PhD scholarships from Asthma New South Wales. V.M. was the recipient of a National Health and Medical Research Council Dora Lush (Biomedical) Postgraduate Scholarship and a Hunter Medical Research Institute/Port Waratah Coal Services Postdoctoral Fellowship. V.C. was the recipient of the Arthur Wilson Memorial Scholarship from the Royal Australian College of Obstetricians and Gynaecologists and National Health and Medical Research Council Career Development Grant (ID 300786). N.S. and A.O.-K. were recipients of Asthma New South Wales postgraduate scholarships.
2 Address correspondence and reprint requests to A/Professor Vicki Clifton, Faculty Health Sciences, School of Paediatrics and Reproductive Health, Medical North, Level 6, Frome Road, University of Adelaide, Adelaide, South Australia, Australia. E-mail address: Vicki.clifton{at}adelaide.edu.au
3 Abbreviations used in this paper: HPA, hypothalamic pituitary adrenal; 11βHSD2, 11 β dehydrogenase type 2; IUGR, intrauterine growth restriction.
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