Chorioamnionitis: A Risk Factor for Fetal and Neonatal Morbidity

Abstract

Despite widespread use of drugs to arrest preterm labor, there has been no decrease in the numbers of low-birth-weight or preterm infants in the last 20 years. Evidence from many sources links preterm birth to symptomatic and subclinical infections. Recently, an increasing body of evidence has suggested that not only is subclinical infection responsible for preterm birth but also for many serious neonatal sequelae, including periventricular leukomalacia, cerebral palsy, respiratory distress and even bronchopulmonary dysplasia and necrotizing enterocolitis. Proxies of intrauterine infection include clinical chorioamnionitis, histological chorioamnionitis and intraamniotic increase in cytokines, which have been found to be associated with acute neonatal morbidity and mortality and, at least to some degree, with neurological impairment, chronic lung disease and thymus involution in the preterm infant. The infectious/inflammatory mechanisms involved are not fully understood, and the types of microbes and genetic features of host adaptive and innate immune responses need to be better characterized.

Selective Impairment of TLR-Mediated Innate Immunity in Human Newborns: Neonatal Blood Plasma Reduces Monocyte TNF-α Induction by Bacterial Lipopeptides, Lipopolysaccharide, and Imiquimod, but Preserves the Response to R-848

“…Because inflammation is known to be an important trigger of premature delivery and its attendant complications (27), we speculate that there may be a selective advantage to having muted neonatal TLR-mediated responses in utero to reduce the risk of inflammatory reactions to maternal and microbial molecules. Such plasma-mediated quenching of signaling via TLRs may protect against inflammation, but may also leave the fetus and newborn at relatively high risk of infection.…”

Chorioamnionitis and neonatal morbidity: current perspectives

“…These morbidities, in turn, have been linked to the development of chronic conditions such as bronchopulmonary dysplasia (BPD) and cerebral palsy (CP) and developmental delay. 3,4 However, a direct causal relationship between CA and these prematurity-related morbidities is still controversial, with some studies showing no effect or even opposite results. The reason for such discrepancies could be the different definitions of CA used in the studies, and the diversity of criteria to include patients.…”

Postnatal administration of IL-1Ra exerts neuroprotective effects following perinatal inflammation and/or hypoxic-ischemic injuries

“…The main causes of such brain injury are perinatal hypoxia-ischaemia (HI) and pathogen-induced inflammation, which are often combined and can have a synergistic effect, mainly through pre-and postnatal release of inflammatory mediators (Boksa, 2010;Bracci and Buonocore, 2003;Ferriero, 2004;Girard et al, 2008;Hagberg et al, 2011;Kapitanović Vidak et al, 2012;Meyer, 2011;Nelson, 2003;Volpe, 2009;Wu et al, 2003). Premature neonates have heightened vulnerability to brain damage.…”