Showing papers by "Bernard M. Babior published in 1988"
TL;DR: The respiratory burst oxidase is an activatable, membrane-bound flavo(?hemo) protein that catalyzes the NADPH-dependent reduction of oxygen to superoxide (O2-) in stimulated phagocytes.
Abstract: The respiratory burst oxidase is an activatable, membrane- bound flavo(?hemo) protein that catalyzes the NADPH- dependent reduction of oxygen to superoxide (O 2 ™) in stimulated phagocytes. Chronic granulomatous disease, a group of disorders in which phagocytes cannot manufacture O 2™, is caused by a biochemical lesion involving this oxidase or its activating system.
365 citations
TL;DR: Neutrophils, the predominant phagocytes of circulating blood, are the first cells to arrive at sites of infection and are recognized to predispose to infection.
Abstract: Neutrophils, the predominant phagocytes of circulating blood, are the first cells to arrive at sites of infection. Although neutropenia has long been recognized to predispose to infection, recently other syndromes marked by frequent infections have been shown to be caused by an underlying neutrophil dysfunction. Efforts to define the molecular pathology of such disorders have helped delineate the molecular basis of normal neutrophil function. Advances have been made in defining the roles of the neutrophil's varied receptors in recognition, movement, and adhesive phenomena. Progress in establishing the pathogenesis of chronic granulomatous disease has provided important insights into the enzymatic machinery that normal neutrophils use to produce antimicrobial oxidants. The identification and precise characterization of antimicrobial components, such as defensins, have outlined the potential roles of "natural antibiotics" in neutrophil-mediated host-defense functions. These areas of neutrophil function will be reviewed and placed in a clinical context to guide physicians in evaluating children and adults with frequent or unusual infections.
348 citations
TL;DR: When 32P-labeled human neutrophils were activated by exposure to phorbol myristate acetate, three 48-kDa proteins were found to have become labeled, providing further evidence for a relationship between the phosphorylation of this group of 48- kDa proteins and the activation of the respiratory burst oxidase.
166 citations
TL;DR: In a fully soluble system from resting human neutrophils, activation of the respiratory burst oxidase under defined conditions was found to follow first-order kinetics.
99 citations
TL;DR: The exposure of 32P-loaded neutrophils to any of a variety of activating agents induces changes in the levels of phosphorylation of a large number of phosphoproteins, which appears to be closely related to the activation of the respiratory burst oxidase, the O2--producing enzyme of phagocytes that is responsible for the generation of microbicidal oxidants by these cells.
76 citations
TL;DR: In all three patients with A/- CGD examined, the two most acidic 48K proteins failed to undergo enhanced phosphorylation in response to phorbol stimulation, a finding similar to that seen in X/- patients.
70 citations
TL;DR: A previously unrecognized role for de novo protein synthesis in maintaining the ability of neutrophils to manufacture O2- is suggested, and earlier studies indicating that the cycling of FMLP receptors between the cell membrane and an intracellular compartment is important in determining the magnitude of the respiratory burst in FMLP-stimulated neutrophiles are supported.
12 citations
TL;DR: The respiratory burst oxidase as discussed by the authors is an enzyme found principally in phagocytes that catalyzes the 1-electron reduction of oxygen to \(O_2^ - \) at the expense of NADPH.
Abstract: The respiratory burst oxidase is an enzyme found principally in phagocytes (Babior 1978; Weiss et al. 1978; Tauber et al. 1979) that catalyzes the 1-electron reduction of oxygen to \(O_2^ - \) at the expense of NADPH:
7 citations
TL;DR: It appears that on exposure to activated neutrophils, a plasmid may acquire a lesion (? mutation) that can somehow be transferred to the genome of a recipient microorganism, resulting in repair of the damaged plasmids accompanied by mutation of the recipient's chromosome.
5 citations