Deacylation of Lipopolysaccharide in Whole Escherichia coli during Destruction by Cellular and Extracellular Components of a Rabbit Peritoneal Inflammatory Exudate

This publication has 43 references indexed in Scilit:

• Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.
  Journal of Clinical Investigation, 1998
• A novel Escherichia coli lipid A mutant that produces an antiinflammatory lipopolysaccharide.
  Journal of Clinical Investigation, 1996
• The potent anti-Staphylococcus aureus activity of a sterile rabbit inflammatory fluid is due to a 14-kD phospholipase A2.
  Journal of Clinical Investigation, 1996
• Lipopolysaccharide (LPS)-binding protein is carried on lipoproteins and acts as a cofactor in the neutralization of LPS.
  The Journal of Experimental Medicine, 1994
• Chylomicrons alter the fate of endotoxin, decreasing tumor necrosis factor release and preventing death.
  Journal of Clinical Investigation, 1993
• Activation of the adhesive capacity of CR3 on neutrophils by endotoxin: dependence on lipopolysaccharide binding protein and CD14.
  The Journal of Experimental Medicine, 1991
• Bacterial phospholipid hydrolysis enhances the destruction of Escherichia coli ingested by rabbit neutrophils. Role of cellular and extracellular phospholipases.
  Journal of Clinical Investigation, 1990
• Structural Requirements of Lipid a for Endotoxicity and Other Biological Activities
  CRC Critical Reviews in Microbiology, 1989
• Biological Activity, Lipoprotein-binding Behavior, and In Vivo Disposition of Extracted and Native Forms of Salmonella typhimurium Lipopolysaccharides
  Journal of Clinical Investigation, 1982
• A RAPID METHOD OF TOTAL LIPID EXTRACTION AND PURIFICATION
  Canadian Journal of Biochemistry and Physiology, 1959