Increased neutrophil respiratory burst in bcr-null mutants

• Published in: Cell Vol. 80; no. 5; pp. 719 - 728
• Main Authors: Voncken, Jan Willem, Schaick, Hermien van, Kaartinen, Vesa, Deemer, Kathleen, Coates, Thomas, Landing, Benjamin, Pattengale, Paul, Dorseuil, Olivier, Bokoch, Gary M, Groffen, John, Heisterkamp, Nora
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 10.03.1995
• Subjects: Actin Cytoskeleton - physiology; Animals; Endotoxins - toxicity; Female; Gene Targeting; GTP-Binding Proteins - biosynthesis; GTP-Binding Proteins - metabolism; Lipopolysaccharides - pharmacology; Male; Mice; Mice, Inbred C57BL; Mutation - physiology; Neutropenia - chemically induced; Neutropenia - immunology; Neutrophil Activation; Neutrophils - metabolism; Oncogene Proteins - genetics; Oncogene Proteins - physiology; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcr; rac GTP-Binding Proteins; Respiratory Burst - immunology; Shock, Septic - chemically induced; Shock, Septic - immunology; Shock, Septic - pathology; Superoxides - metabolism; Toxemia - chemically induced; Toxemia - immunology; Toxemia - pathology

Philadelphia (Ph)-positive leukemias invariably contain a chromosomal translocation fusing BCR to ABL. The BCR-ABL protein is responsible for leukemogenesis. Here we show that exposure of bcr-null mutant mice to gram-negative endotoxin led to severe septic shock and increased tissue injury by neutro...