REVIEW ARTICLE published: 01 December 2014 doi: 10.3389/fimmu.2014.00574
Preterm birth, intrauterine infection, and fetal inflammation Matthew W. Kemp* School of Women’s and Infants’ Health, The University of Western Australia, Perth, WA, Australia
Edited by: Claudia Monaco, Catholic University Rome & Imperial College, UK Reviewed by: Marian Kacerovsky, University Hospital in Prague, Czech Republic Ana María Franchi, The National Scientific and Technical Research Council (CONICET), Argentina *Correspondence: Matthew W. Kemp, School of Women’s and Infants’ Health, The University of Western Australia, M550, 35 Stirling Highway, Crawley, Perth WA 6009, Australia e-mail: [email protected]
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 pathologies associated with prematurity. As such, a better understanding of intrauterine inflammation in pregnancy is critical to our understanding of preterm labor and fetal injury, as well as on-going efforts to prevent PTB. Focusing on the fetal innate immune system responses to intrauterine infection, the present paper will review clinical and experimental studies to discuss the capacity for a fetal contribution to the intrauterine inflammation associated with PTB. Evidence from experimental studies to suggest that the fetus has the capacity to elicit a pro-inflammatory response to intrauterine infection is highlighted, with reference to the contribution of the lung, skin, and gastrointestinal tract. The paper will conclude that pathological intrauterine inflammation is a complex process that is modified by multiple factors including time, type of agonist, host genetics, and tissue. Keywords: preterm birth, fetus, inflammation, infection, injury
INTRODUCTION Preterm birth (PTB) is presently defined as delivery before 37 weeks’ completed gestation from the last known menstrual period (1); the lower limit of PTB varies between countries but is generally set at 20 or 22 weeks’ completed gestation (2). PTB is often further sub-classified into late (32 or 34–36 completed weeks’ gestation), early (
Preterm birth, intrauterine infection, and fetal inflammation Matthew W. Kemp* School of Women’s and Infants’ Health, The University of Western Australia, Perth, WA, Australia
Edited by: Claudia Monaco, Catholic University Rome & Imperial College, UK Reviewed by: Marian Kacerovsky, University Hospital in Prague, Czech Republic Ana María Franchi, The National Scientific and Technical Research Council (CONICET), Argentina *Correspondence: Matthew W. Kemp, School of Women’s and Infants’ Health, The University of Western Australia, M550, 35 Stirling Highway, Crawley, Perth WA 6009, Australia e-mail: [email protected]
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 pathologies associated with prematurity. As such, a better understanding of intrauterine inflammation in pregnancy is critical to our understanding of preterm labor and fetal injury, as well as on-going efforts to prevent PTB. Focusing on the fetal innate immune system responses to intrauterine infection, the present paper will review clinical and experimental studies to discuss the capacity for a fetal contribution to the intrauterine inflammation associated with PTB. Evidence from experimental studies to suggest that the fetus has the capacity to elicit a pro-inflammatory response to intrauterine infection is highlighted, with reference to the contribution of the lung, skin, and gastrointestinal tract. The paper will conclude that pathological intrauterine inflammation is a complex process that is modified by multiple factors including time, type of agonist, host genetics, and tissue. Keywords: preterm birth, fetus, inflammation, infection, injury
INTRODUCTION Preterm birth (PTB) is presently defined as delivery before 37 weeks’ completed gestation from the last known menstrual period (1); the lower limit of PTB varies between countries but is generally set at 20 or 22 weeks’ completed gestation (2). PTB is often further sub-classified into late (32 or 34–36 completed weeks’ gestation), early (
