Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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-alpha production in the THP-1 cell line stimulated by lipopolysaccharide 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-alpha 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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PMID:Inhibition of macrophage proinflammatory cytokine expression by steroids and recombinant IL-10. 1150 12

Cystic fibrosis (CF) is a complex multisystem disorder caused by mutations in a membrane glycoprotein called the CF transmembrane regulator (CFTR), which has as its major function serving as a Cl- channel. The relationship between defects in CFTR and development of lung disease remains incompletely understood. Chronic lung disease, characterized by persistent infection with a peculiar type of Pseudomonas aeruginosa, bronchiectasis, and airway obstruction is the major cause of morbidity and mortality in CF patients. The inflammatory response to the chronic infection resembles that induced by lipopolysaccharide (LPS) and is mediated primarily by cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-6, and IL-8, whose synthesis is activated by the transcription factor nuclear factor kappa B (NF-kappa B). Large numbers of neutrophils dominate the inflammatory response and excessive concentrations of their products create a vicious cycle that becomes injurious rather than protective and eventually claims the life of the patient.
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PMID:Inflammatory mediators in cystic fibrosis lung disease. 1189 30