Lipopolysaccharide binding protein enhances the responsiveness of alveolar macrophages to bacterial lipopolysaccharide. Implications for cytokine production in normal and injured lungs.

摘要: A plasma lipopolysaccharide (LPS)-binding protein (LBP) has been shown to regulate the response of rabbit peritoneal macrophages and human blood monocytes endotoxin (LPS). We investigated whether LBP is present in lung fluids effects on LPS. Immunoreactive was detectable lavage patients with adult respiratory distress syndrome by immunoprecipitation followed Western blotting, also specific immunoassay. In rabbits, appeared originate outside lungs, inasmuch as mRNA transcripts for were identified total cellular RNA from liver, but not homogenates or alveolar macrophages. Purified enhanced both smooth form LPS (Escherichia coli O111B:4) rough (Salmonella minnesota Re595). presence LPS, onset tumor necrosis factor-alpha (TNF alpha) production occurred earlier at an threshold dose that much 1,000-fold lower types treated TNF alpha earlier, reached higher levels, had a prolonged half-life compared treatment alone. Neither nor affected pHi [Cai++] Specific monoclonal antibodies CD14, receptor binds LPS/LBP complexes, inhibited stimulated alone indicating importance CD14 mediating Thus, immunoreactive accumulates injury enhances LPS-stimulated gene expression pathway depends receptor. may play important role augmenting within lungs.