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Published on: November 20, 2015
Antenatal inflammation and infection in chronic lung disease of prematurity
R E Miralles1, R Hodge, S Kotecha
1Department of Child Health, University of Leicester, Leicester, UK.
Insights
Chronic lung disease (CLD) in preterm infants is linked to antenatal inflammation and infection. Further research using molecular techniques may clarify the role of Ureaplasma urealyticum in CLD pathogenesis.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Infectious Disease
Background:
- Chronic lung disease (CLD) remains a significant cause of death and illness in extremely preterm infants despite advances in neonatal care.
- Antenatal infection and inflammation are increasingly recognized as factors contributing to preterm birth and potentially increasing CLD susceptibility.
- Pro-inflammatory cytokine exposure in the fetal lung is hypothesized to play a role in the development of CLD.
Purpose of the Study:
- To explore the link between antenatal infection, intra-uterine inflammation, and the development of CLD in preterm infants.
- To investigate the potential role of Ureaplasma urealyticum (Uu) as an initiator of intra-uterine inflammation and its association with CLD.
- To review the current evidence on antibiotic interventions for mothers and preterm infants in relation to CLD outcomes.
Main Methods:
- Literature review and synthesis of current research on antenatal infection, inflammation, and CLD.
- Discussion of the potential role of Ureaplasma urealyticum (Uu) in the pathogenesis of CLD.
- Evaluation of the efficacy of antibiotic treatments in mothers and neonates concerning CLD prevention and management.
Main Results:
- Antenatal infection can trigger inflammation, leading to preterm labor and potentially increasing CLD risk in neonates.
- Antibiotic use in mothers before delivery shows benefit for prolonged rupture of membranes but not for preterm labor with intact membranes.
- The vertical transmission of Uu to preterm infants and its definitive role in causing CLD remain uncertain, with limited consistent benefits observed from postnatal antibiotic trials.
Conclusions:
- CLD remains a critical issue for extremely preterm infants.
- Molecular biology techniques, such as PCR, are expected to improve the detection of antenatal infections.
- Enhanced detection methods will likely advance the understanding of CLD pathogenesis and inform future prevention strategies.
Abstract:
In spite of improved neonatal care, chronic lung disease of prematurity (CLD) remains a major cause of morbidity and mortality in extremely preterm infants. Our current understanding is that antenatal infection can trigger intra-uterine inflammation which then promotes preterm labour. Recent studies suggest that antenatal infection and inflammation can also increase the preterm infant's susceptibility to develop CLD. It may be that exposure of the fetal lung to high concentrations of pro-inflammatory cytokines is the cause of this increased susceptibility. One candidate for initiating intra-uterine inflammation is ascending infection by the vaginal commensal Ureaplasma urealyticum (Uu). Antibiotics administered to mothers prior to delivery appear to improve the neonatal outcome in cases of preterm prolonged rupture of membranes, but not in cases of preterm labour with intact membranes. Uu can be transmitted vertically to the airways of the preterm infant, but the role of Uu in causing CLD remains uncertain. Small trials of antibiotics given to preterm infants after delivery have not shown any consistent benefit in reducing CLD. Although CLD remains a significant problem for the extremely preterm infant, it is likely that molecular biology techniques, such as the polymerase chain reaction, will enhance the detection of antenatal infection and further our understanding of the pathogenesis of CLD.
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