Induction of TNF-alpha release from human buffy coat cells by Pseudomonas aeruginosa is reduced by lung surfactant protein A.
Lipopolysaccharide (LPS) induction of TNF-alpha release is a central event in the pathophysiology of gram-negative bacterial septicaemia. Lung surfactant protein A (SP-A) mediates pathogen/host cell interactions. Binding of SP-A to Pseudomonas aeruginosa LPS and the effects of SP-A with LPS or whole bacteria on buffy coat cells were investigated. SP-A interacts with P. aeruginosa LPS in a concentration and calcium dependent manner, either through the lipid A portion of LPS or through another lectin/carbohydrate interaction. SP-A decreased TNF-alpha secretion induced by bacteria or LPS from buffy coat cells, in a concentration dependent manner.
Hickling
T P
TP
Department of Biochemistry, University of Oxford, UK.
Sim
R B
RB
Malhotra
R
R
D001059:Apoproteins / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D007962:Leukocytes / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism / Q000494:pharmacology*; D011550:Pseudomonas aeruginosa / Q000378:metabolism*; D037661:Pulmonary Surfactant-Associated Proteins; D011663:Pulmonary Surfactants / Q000378:metabolism / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D001059:Apoproteins; D008070:Lipopolysaccharides; D037661:Pulmonary Surfactant-Associated Proteins; D011663:Pulmonary Surfactants; D014409:Tumor Necrosis Factor-alpha; C082161:lipopolysaccharide A; C046616:pulmonary surfactant apoprotein