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J Leukoc Biol. 2016 Jan;99(1):67-78. doi: 10.1189/jlb.3MR0615-272RR. Epub 2015 Nov 4.

Inflammation and preterm birth.

Author information

1
*Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; Unit of Clinical and Experimental Immunology, Humanitas Clinical and Research Center, Rozzano, Italy; and Department of Woman, Mother and Neonate, Buzzi Children's Hospital, Biomedical and Clinical Sciences School of Medicine, University of Milan, Italy.
2
*Division of Immunobiology, Cincinnati Children's Hospital Research Foundation, and the University of Cincinnati College of Medicine, Cincinnati, Ohio, USA; Unit of Clinical and Experimental Immunology, Humanitas Clinical and Research Center, Rozzano, Italy; and Department of Woman, Mother and Neonate, Buzzi Children's Hospital, Biomedical and Clinical Sciences School of Medicine, University of Milan, Italy senad.divanovic@cchmc.org.

Abstract

Preterm birth is the leading cause of neonatal morbidity and mortality. Although the underlying causes of pregnancy-associated complication are numerous, it is well established that infection and inflammation represent a highly significant risk factor in preterm birth. However, despite the clinical and public health significance, infectious agents, molecular trigger(s), and immune pathways underlying the pathogenesis of preterm birth remain underdefined and represent a major gap in knowledge. Here, we provide an overview of recent clinical and animal model data focused on the interplay between infection-driven inflammation and induction of preterm birth. Furthermore, here, we highlight the critical gaps in knowledge that warrant future investigations into the interplay between immune responses and induction of preterm birth.

KEYWORDS:

Toll-like receptors; cytokines; infection; innate immune cells

PMID:
26538528
DOI:
10.1189/jlb.3MR0615-272RR
[Indexed for MEDLINE]

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