We are very pleased that our paper has stirred so much thought and attention. We fully agree that vitamin D deficiency as a factor associated with bacterial vaginosis and susceptibility to infection should be thoroughly studied to explore its potential role as an easily modifiable cause of preterm birth and complications of prematurity (1). We hope future studies will address that.
To clarify, in our paper we investigated placental colonization with specific groups of bacteria as a mechanism to upregulate or downregulate the inflammatory condition in the extremely preterm newborn rather than as a risk factor for or a trigger of premature birth (2). The ELGAN study did not assess maternal levels of vitamin D.
It may well be that vitamin D deficiency affects fetal growth and development through its direct effect on systemic and mucosal innate immunity and inflammation (3–5) or through control of the growth, composition, ascendance, and pathogenicity of the maternal microflora (6). We and others continue to search for new ways to reduce the heavy burden of preterm birth for millions of children and families.
Raina N. Fichorova
Laboratory of Genital Tract Biology
Department of Obstetrics and Gynecology
Harvard Medical School and Brigham and Women's Hospital
Boston, Massachusetts, USA
Andrew B. Onderdonk
Department of Pathology
Harvard Medical School and Brigham and Women’s Hospital
Boston, Massachusetts, USA
Hidemi Yamamoto
Laboratory of Genital Tract Biology
Department of Obstetrics and Gynecology
Harvard Medical School and Brigham and Women's Hospital
Boston, Massachusetts, USA
Mary L. Delaney
Andrea M. DuBois
Department of Pathology
Harvard Medical School and Brigham and Women’s Hospital
Boston, Massachusetts, USA
Elizabeth Allred
Alan Leviton
Neuroepidemiology Unit
Children’s Hospital of Boston
Boston, Massachusetts, USA
- Copyright © 2011 Fichorova et al.
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