Yaling Xu1, Ying Dong2, Xiaojing Guo1, Bo Sun3. 1. Laboratory of Pediatric Respiratory and Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China. 2. Department of Neonatology, Children's Hospital of Fudan University, Shanghai, China. 3. Laboratory of Pediatric Respiratory and Critical Care Medicine, Children's Hospital of Fudan University, Shanghai, China. bsun@shmu.edu.cn.
Abstract
BACKGROUND: The pathogenesis of neonatal group B Streptococcus (GBS) lung infection may be associated with surfactant dysfunction or deficiency. This study aimed to investigate the efficacy of surfactants on early postnatal GBS infection in ventilated newborn rabbit lungs. METHODS: A near-term newborn rabbit model was established by intratracheal GBS instillation immediately at birth, followed by mechanical ventilation. At postnatal 1 h, a porcine surfactant was given intratracheally at 100 or 200 mg/kg. After 6 h, animals were euthanized, and lung and blood samples were collected for bacterial counting. Lung histopathology and messenger RNA (mRNA) expression of inflammatory mediators, surfactant proteins, and growth factors in lung tissue were assessed. RESULTS: The surfactants significantly suppressed (by >50%) pulmonary bacterial proliferation and systemic translocation, alleviated lung inflammatory injury, and improved alveolar expansion by morphometry, in favor of high-dose surfactants. Though the survival rate and lung mechanics were not improved, the surfactants significantly suppressed mRNA expression of proinflammatory mediators, while that for surfactant proteins and growth factors was differentially expressed, compared to the control and GBS infection groups. CONCLUSION: Exogenous surfactants may provide a therapeutic alternative for neonatal lung infection by suppressing pulmonary GBS proliferation and translocation into systemic circulation, alleviating inflammatory injury and regulating growth factor expression.
BACKGROUND: The pathogenesis of neonatal group B Streptococcus (GBS) lung infection may be associated with surfactant dysfunction or deficiency. This study aimed to investigate the efficacy of surfactants on early postnatal GBS infection in ventilated newborn rabbit lungs. METHODS: A near-term newborn rabbit model was established by intratracheal GBS instillation immediately at birth, followed by mechanical ventilation. At postnatal 1 h, a porcine surfactant was given intratracheally at 100 or 200 mg/kg. After 6 h, animals were euthanized, and lung and blood samples were collected for bacterial counting. Lung histopathology and messenger RNA (mRNA) expression of inflammatory mediators, surfactant proteins, and growth factors in lung tissue were assessed. RESULTS: The surfactants significantly suppressed (by >50%) pulmonary bacterial proliferation and systemic translocation, alleviated lung inflammatory injury, and improved alveolar expansion by morphometry, in favor of high-dose surfactants. Though the survival rate and lung mechanics were not improved, the surfactants significantly suppressed mRNA expression of proinflammatory mediators, while that for surfactant proteins and growth factors was differentially expressed, compared to the control and GBS infection groups. CONCLUSION: Exogenous surfactants may provide a therapeutic alternative for neonatal lung infection by suppressing pulmonary GBS proliferation and translocation into systemic circulation, alleviating inflammatory injury and regulating growth factor expression.