BioProject

Introduction: Increasing evidence now supports the association between the fetal inflammatory response syndrome (FIRS) with the pathogenesis of preterm labor, intraventricular hemorrhage and bronchopulmonary dysplasia. More...

Introduction: Increasing evidence now supports the association between the fetal inflammatory response syndrome (FIRS) with the pathogenesis of preterm labor, intraventricular hemorrhage and bronchopulmonary dysplasia. These disorders are among the most important causes of mortality and morbidity in the perinatal period. During the fetal inflammatory response syndrome (FIRS) polymorphonuclear leukocytes (PMNs) and monocytes (MONOs) are sequentially recruited into the placenta; the same process occurs in the lung of the newborn during the development of bronchopulmonary dysplasia (BPD). The aim of the study was to reveal cell-specific differences in gene expression and cytokine release in response to endotoxin that would elucidate inflammatory control mechanisms in the newly born. Results: Compared to PMNs, MONOs had a greater diversity and more robust expression of pro-inflammatory (PI) gene expression at 4h. Only MONOs had genes changing expression in the JAK/STAT pathway including interleukin-10. Overall design: Isolation of cord blood polymorphonuclear leukocytes and monocytes separately from 5 subjects. Endotoxin stimulation in cell culture for 4 hours. Comparison of gene expression between PBS versus endotoxin (LPS). Less...