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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
The role of inflammation in the development of chronic lung disease in neonates
J J De Dooy1, L M Mahieu, H P Van Bever
1Department of Paediatrics, University Hospital of Antwerp, Belgium. jozef.dedooy@uia.ua.ac.be
Insights
Inflammation is critical in neonatal chronic lung disease (CLD). Early anti-inflammatory therapy may prevent CLD, but more research is needed to identify high-risk infants.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Immunology
Background:
- Chronic lung disease (CLD) in neonates is linked to chorioamnionitis and Ureaplasma urealyticum colonization.
- Inflammation is increasingly recognized as a key factor in the early development of CLD.
- Failure to regulate inflammatory responses may cause ongoing lung damage in premature infants.
Purpose of the Study:
- To review evidence on the role of inflammation in neonatal CLD.
- To explore potential therapeutic strategies targeting inflammation.
- To highlight areas requiring further research.
Main Methods:
- Literature review of studies on neonatal CLD pathogenesis.
- Analysis of the role of pro-inflammatory cytokines (TNF-alpha, IL-6, IL-8) and anti-inflammatory cytokine (IL-10).
- Evaluation of potential interventions and modulating factors.
Main Results:
- Pro-inflammatory cytokines like IL-8 are crucial in lung inflammation.
- Preterm infants may have impaired ability to activate the anti-inflammatory cytokine IL-10.
- Early anti-inflammatory therapy is a potential strategy for CLD prevention, though prophylactic dexamethasone is not yet recommended.
Conclusions:
- The precise inflammatory pathways in CLD pathogenesis require further elucidation.
- Identifying preterm infants at highest risk for CLD is essential for targeted interventions.
- Further research is needed on the complex, multifactorial nature of CLD.
Unlabelled:
Chronic lung disease (CLD) has been associated with chorioamnionitis and upper respiratory tract colonisation with Ureaplasma urealyticum. The aim of this review is to describe the increasing evidence that inflammation plays a critical role in the early stages of CLD of the neonate. Ongoing lung damage in the premature infant may be caused by failure to downregulate and control this inflammatory response. Tumour necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6) and IL-8 are important pro-inflammatory cytokines of which IL-8 is an important chemotactic factor in the lung. Data suggest that preterm newborns with lung inflammation may be unable to activate the anti-inflammatory cytokine IL-10. Therefore, early post-natal anti-inflammatory therapy could help in preventing development of CLD. Prophylactic dexamethasone therapy cannot yet be recommended. There are a number of potential interactions between surfactant and cytokine effects on the preterm lung which have not been evaluated. Surfactant protein A may be an important modulator of the immune response to lung injury. The role of high-frequency ventilation in the prevention of CLD still remains unclear.
Conclusion:
Many aspects of the pathogenesis of the inflammatory response in the development of chronic lung disease remain to be elucidated. Further research to identify preterm infants at highest risk for the development of this multifactorial and complex disease is needed.
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