IL-1 Mediates Pulmonary and Systemic Inflammatory Responses to Chorioamnionitis Induced by Lipopolysaccharide
| Autor: | Fook-Choe Cheah, John P. Newnham, Boris W. Kramer, Alan H. Jobe, J. Jane Pillow, Timothy J. M. Moss, Suhas G. Kallapur, Machiko Ikegami, Graeme R. Polglase, Ilias Nitsos |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Lipopolysaccharides
Pulmonary and Respiratory Medicine Lipopolysaccharide Interleukin-1beta Enzyme-Linked Immunosorbent Assay Inflammation Critical Care and Intensive Care Medicine Chorioamnionitis Systemic inflammation chemistry.chemical_compound Fetus Pregnancy Interleukin-1alpha medicine Animals Humans Lung Sheep Respiratory distress F. Pediatrics and Lung Development business.industry Respiratory disease Receptors Interleukin-1 Pneumonia medicine.disease Recombinant Proteins Disease Models Animal Interleukin 1 Receptor Antagonist Protein medicine.anatomical_structure chemistry Immunology Female medicine.symptom business Bronchoalveolar Lavage Fluid Signal Transduction |
| Zdroj: | American Journal of Respiratory and Critical Care Medicine. 179:955-961 |
| ISSN: | 1535-4970 1073-449X |
| DOI: | 10.1164/rccm.200811-1728oc |
| Popis: | Chorioamnionitis frequently associates with preterm delivery and increased amniotic fluid IL-1, and causes fetal lung and systemic inflammation. However, chorioamnionitis is also associated with a paradoxical reduction in the incidence of surfactant deficiency-related respiratory distress syndrome in preterm infants.To identify the role of IL-1 signaling in the mediation of pulmonary and systemic inflammation and lung maturation in a fetal sheep model of lipopolysaccharide (LPS) induced chorioamnionitis.After confirming the efficacy of recombinant human IL-1 receptor antagonist (rhIL-1ra), fetal sheep were exposed to intraamniotic (IA) injections of Escherichia coli LPS with or without prior IA injections of rhIL-1ra. Preterm lambs were delivered at 82% of term gestation.rhIL-1ra decreased IA LPS-induced lung inflammation assessed by decreased lung neutrophil and monocyte influx, inducible nitric oxide synthase expression, lung IL-6 and IL-1beta mRNA expression, and airway myeloperoxidase concentrations. rhIL-1ra inhibited IA LPS-induced fetal systemic inflammation assessed by decreased plasma IL-8, protein carbonyls, blood neutrophilia, and the expression of serum amyloid A3 mRNA in the liver. rhIL-1ra also partially blocked the lung maturational effects of IA LPS. Therefore blockade of IL-1 signaling in the amniotic compartment inhibited fetal lung and systemic inflammation and lung maturation in response to LPS-induced chorioamnionitis.IL-1 plays a central role in the pathogenesis of chorioamnionitis-induced fetal inflammatory responses. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|