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- Li, YH, et al.
(author)
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Induction of human macrophage vascular endothelial growth factor and intercellular adhesion molecule-1 by Ureaplasma urealyticum and downregulation by steroids
- 2002
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In: Biology of the neonate. - : S. Karger AG. - 0006-3126. ; 82:1, s. 22-28
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Journal article (peer-reviewed)abstract
- Chronic lung disease (CLD) remains a major cause of morbidity for the prematurely born infant. The pathogenesis of CLD is complex and has not been defined entirely. Infection and lung inflammatory events have been thought to play a key role in the development of CLD. However, the contribution of <i>Ureaplasma urealyticum</i> to the development of CLD is debated and steroids produce some improvement in neonates with this disease. The aim of this study was to investigate if <i>U. urealyticum</i> could stimulate macrophages to produce vascular endothelial growth factor (VEGF) and intercellular adhesion molecule-1 (ICAM-1) in vitro, which are potentially associated with both early and later pathological changes in the lung during the development of CLD. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that <i>U. urealyticum</i> antigen (≧4 × 10<sup>7</sup> color-changing units/ml) stimulated human macrophages (phorbol 12-myristate 13-acetate-differentiated THP-1 cell line) to produce VEGF and soluble ICAM-1 in a dose-dependent manner (p < 0.05) measured by ELISA. Likewise, cell surface ICAM-1 (CD54) measured by flow cytometry was increased after stimulation with <i>U. urealyticum</i>. This effect was attenuated by budesonide and dexamethasone (p < 0.05). The mRNA expressions of VEGF and ICAM-1 detected by a semi-quantitative reverse transcriptase polymerase chain reaction were also induced in response to <i>U. urealyticum</i> and inhibited by the steroids (p < 0.05). The expression of ICAM-1 was reduced by 85.5% when the TNF-α production was neutralized with an anti-TNF-α antibody. Our findings imply that <i>U. urealyticum </i>might be involved in the development of CLD of prematurity.
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- Li, YH, et al.
(author)
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Inhibition of macrophage proinflammatory cytokine expression by steroids and recombinant IL-10
- 2001
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In: Biology of the neonate. - : S. Karger AG. - 0006-3126. ; 80:2, s. 124-132
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Journal article (peer-reviewed)abstract
- Chronic lung disease (CLD) of prematurity is a prolonged respiratory failure in very-low-birth-weight neonates. Proinflammatory cytokines have been implicated in the development of CLD. Steroids have been shown to produce some improvement in neonates with this disease. The purpose of this study was to evaluate the downregulation of these proinflammatory cytokines by dexamethasone, budesonide and recombinant IL-10 (rIL-10) in order to elucidate the mechanism of the clinical benefit of steroids in babies. Our results showed that dexamethasone, budesonide and rIL-10 significantly inhibited both IL-6 and TNF-α production in the THP-1 cell line stimulated by lipopolysaccharide and <i>Ureaplasma urealyticum</i> 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-α production, while rat rIL-10 did not significantly decrease production. In conclusion, steroids and human rIL-10 were able to downregulate proinflammatory cytokine production, which may explain the beneficial effect of steroids and suggests that rIL-10 could be tried as an anti-inflammatory agent in neonates with a high risk of CLD.
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