Extracellular Vesicles-mediated recombinant IL-10 protects against ascending infection-associated preterm birth by reducing fetal inflammatory response

Hyaluronan in cervical epithelia protects against infection-mediated preterm birth.

Increased synthesis of cervical hyaluronan (HA) from early to late pregnancy has long been proposed to play an essential role in disorganization of the collagen-rich extracellular matrix to allow for maximal compliance and dilation of the cervix during the birth process. Here, we show that HA is not essential for increased cervical distensibility during late pregnancy. Rather, cervicovaginal HA...

Preterm Birth, Intrauterine Infection, and Fetal Inflammation

Preterm birth (PTB) (delivery before 37 weeks' gestation) is a leading cause of neonatal death and disease in industrialized and developing countries alike. Infection (most notably in high-risk deliveries occurring before 28 weeks' gestation) is hypothesized to initiate an intrauterine inflammatory response that plays a key role in the premature initiation of labor as well as a host of the path...

Intestinal Reperfusion Injury Acute Inflammatory Response Following Protects Against the Systemic and Local IL-1-Driven Endogenous IL-10 Production

Bacterial Hyaluronidase Promotes Ascending GBS Infection and Preterm Birth

UNLABELLED Preterm birth increases the risk of adverse birth outcomes and is the leading cause of neonatal mortality. A significant cause of preterm birth is in utero infection with vaginal microorganisms. These vaginal microorganisms are often recovered from the amniotic fluid of preterm birth cases. A vaginal microorganism frequently associated with preterm birth is group B streptococcus (GBS...

Pathogenesis to Treatment: Preventing Preterm Birth Mediated by Infection

Prevention of preterm birth and subsequent newborn immaturity is a primary goal of obstetrical care worldwide. Accumulated evidence shows that 1) as many as 25-50% of preterm births are caused by common genital tract infections and subsequent maternal/fetal inflammatory responses; 2) microbial and maternal host factors (phospholipases, proteases, etc.) play roles in preterm labor and preterm pr...