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Reply to “Adequate Vitamin D during Pregnancy Reduces the Risk of Premature Birth by Reducing Placental Colonization by Bacterial Vaginosis Species”

Raina Nakova Fichorova, Andrew Bruce Onderdonk, Hidemi S. Yamamoto, Mary L. Delaney, Andrea M DuBois, Elizabeth N. Allred, Alan Edward Leviton

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Abstract

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. ItmaywellbethatvitaminDdeficiencyaffectsfetalgrowthand 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 newwaystoreducetheheavyburdenofpretermbirthformillions of children and families.

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What this paper is about

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. ItmaywellbethatvitaminDdeficiencyaffectsfetalgrowthand 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 newwaystoreducetheheavyburdenofpretermbirthformillions of children and families.

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Available abstract

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. ItmaywellbethatvitaminDdeficiencyaffectsfetalgrowthand 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 newwaystoreducetheheavyburdenofpretermbirthformillions of children and families.

Key concepts: Bacterial vaginosis, Premature birth, Pregnancy, Colonization, Medicine, Obstetrics, Placenta, Biology

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