title: Lipopolysaccharides stimulate Na-dependent transport in alveolar cells and protect against oxidant injury.
abstract: We have evaluated the effect of lipopolysaccharides (LPS), endotoxins from gram negative bacteria, on sodium-coupled amino acid and phosphate transport by alveolar epithelial type II cells and on their alteration induced by oxidants. Alveolar type II cells were obtained by enzymatic digestion of rat lung and grown for 24 h prior to incubation with LPS and then exposed or not exposed to H2O2 (2.5 mM; 20 min). LPS (10 micrograms/ml, 24 h) induced a significant increase in the Na-dependent component of alanine and phosphate uptake while they decreased Na,K-ATPase activity measured by ouabain-sensitive 86Rb influx. We showed that this stimulatory effect i) was independent from macrophage products since it was not mimicked either by supernatant of LPS-treated alveolar macrophages or by pretreatment with tumor necrosis factor and/or interleukin 1 and ii) was dependent on protein synthesis since it was abolished by protein synthesis inhibitors cycloheximide and actinomycin D. Moreover, LPS blunted H2O2-induced decrease of Na-dependent alanine and phosphate uptake. This protective effect of LPS against H2O2 injury i) was independent of macrophage products, ii) was abolished by cycloheximide, and iii) was not associated with either changes in extracellular H2O2 clearance or catalase and glutathione peroxidase activities. We conclude that, in alveolar type II cells, LPS stimulate sodium-coupled transport by a process involving protein synthesis and partially prevent H2O2-induced decrease of Na-coupled transport without discernible change in antioxidant activities.
authors.affiliation: Department of Physiology, Faculté de Médecine Xavier Bichat, Université Denis Diderot-Paris, France.
authors.forename: R
authors.initials: R
authors.lastname: Azarian
authors.forename: C
authors.initials: C
authors.lastname: Clerici
authors.forename: S
authors.initials: S
authors.lastname: Couette
authors.forename: G
authors.initials: G
authors.lastname: Friedlander
authors.forename: C
authors.initials: C
authors.lastname: Amiel
mesh_terms: D000409:Alanine / Q000037:antagonists & inhibitors / Q000378:metabolism*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001692:Biological Transport / Q000187:drug effects; D002794:Choline / Q000378:metabolism; D004247:DNA / Q000096:biosynthesis; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007930:Leucine / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000378:metabolism; D010710:Phosphates / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism; D011650:Pulmonary Alveoli / Q000166:cytology / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000502:physiology*
chemical_list: D000975:Antioxidants; D008070:Lipopolysaccharides; D010710:Phosphates; D011506:Proteins; D004247:DNA; D012964:Sodium; D006861:Hydrogen Peroxide; D007930:Leucine; D002794:Choline; D000409:Alanine