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  • Li, YH, et al. (författare)
  • Inhibition of macrophage proinflammatory cytokine expression by steroids and recombinant IL-10
  • 2001
  • Ingår i: Biology of the neonate. - : S. Karger AG. - 0006-3126. ; 80:2, s. 124-132
  • Tidskriftsartikel (refereegranskat)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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  • Li, YH, et al. (författare)
  • Ureaplasma urealyticum induces apoptosis in human lung epithelial cells and macrophages
  • 2002
  • Ingår i: Biology of the neonate. - : S. Karger AG. - 0006-3126. ; 82:3, s. 166-173
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic lung disease (CLD) of prematurity remains a significant cause of morbidity among premature infants. It is a multifactorial disorder and characterized by an early increased number of neutrophils and alveolar macrophages, with later architectural epithelial and endothelial cell damage. Recently, apoptosis of type 2 pneumocytes in the lung of preterm neonates with acute and chronic lung disease has been examined and apoptosis of mesenchymal cells was detected in the chronic stage of bronchopulmonary dysplasia. Infection and inflammatory responses in the lungs play important roles. However, the contribution of <i>Ureaplasma urealyticum</i> to the development of CLD is debated. We found that <i>U. urealyticum</i> induced apoptosis in human type II lung epithelial cells (A549 cell line) and macrophages (derived from human monocytic cell line THP-1) by measuring the outer leaflets translocation of phosphatidylserine (flow cytometry analysis and fluorescence microscopy assessment), DNA fragmentation analysis, cell morphology changes such as diminution in cell volume, increased cytoplasmic staining, and nuclear pyknosis (hematoxylin and eosin staining) and viable counting (trypan blue exclusion). Anti-TNF-α monoclonal antibody partially protected the macrophages from undergoing apoptosis after infection with <i>U. urealyticum.</i> Our findings imply that <i>U. urealyticum</i> might be involved in impairing lung structure and host immune response during the development of CLD.
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  • Resultat 21-30 av 38

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