Inhibition of macrophage proinflammatory cytokine expression by steroids and recombinant IL-10

Chronic lung disease (CLD) of prematurity is a prolonged respiratory failur e in very-low-birth-weight neonates. Proinflammatory cytokines have been im plicated in the development of CLD. Steroids have been shown to produce som e improvement in neonates with this disease. The purpose of this study was to evaluate the downregulation of these proinflammatory cytokines by dexame thasone, budesonide and recombinant IL-10 (rIL-10) in order to elucidate th e mechanism of the clinical benefit of steroids in babies. Our results show ed that dexamethasone, budesonide and rIL-10 significantly inhibited both I L-6 and TNF-alpha production in the THP-1 cell line stimulated by lipopolys accharide and Ureaplasma urealyticum antigen. Similar effects were found in macrophages from tracheobronchial aspirate fluid from newborn infants. In the rat alveolar macrophage cell line, steroids inhibited IL-6 and TNF-a pr oduction, while rat rIL-10 did not significantly decrease production. In co nclusion, steroids and human rIL-10 were able to downregulate proinflammato ry cytokine production, which may explain the beneficial effect of steroids and suggests that rIL-10 could be tried as an anti-inflammatory agent in n eonates with a high risk of CLD. Copyright (C) 2001 S. Karger AG, Basel.