Inflammation and preterm birth

被引:229
作者
Cappelletti, Monica [1 ,2 ]
Della Bella, Silvia [3 ]
Ferrazzi, Enrico [4 ]
Mavilio, Domenico [3 ]
Divanovic, Senad [1 ,2 ]
机构
[1] Cincinnati Childrens Hosp Res Fdn, Div Immunobiol, Cincinnati, OH USA
[2] Univ Cincinnati, Coll Med, Cincinnati, OH USA
[3] Humanitas Clin & Res Ctr, Unit Clin & Expt Immunol, Rozzano, Italy
[4] Univ Milan, Dept Woman Mother & Neonate, Buzzi Childrens Hosp, Biomed & Clin Sci Sch Med, I-20122 Milan, Italy
关键词
infection; Toll-like receptors; cytokines; innate immune cells; TOLL-LIKE RECEPTORS; TUMOR-NECROSIS-FACTOR; SYSTEMIC-LUPUS-ERYTHEMATOSUS; MATERNAL-FETAL INTERFACE; HUMAN NK CELLS; DENDRITIC CELLS; UREAPLASMA-UREALYTICUM; PREMATURE RUPTURE; AMNIOTIC-FLUID; ANIMAL-MODELS;
D O I
10.1189/jlb.3MR0615-272RR
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:67 / 78
页数:12
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