Oxygen-Dependent Microbial Killing by Phagocytes

Babior, Bernard M.

doi:10.1056/nejm197803232981205

Cited by 2,282 publications

(664 citation statements)

References 81 publications

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“…It is believed that the enhanced capability of activated macrophages to resist infection [17] and destroy tumours [18,19] is related to the remarkable increase in the production of oxygen metabolites in response to phagocytosis. Monocytes play a crucial role in host defence by generating microbicidal oxygen metabolites including superoxide (O 2 2 ), hydrogen peroxide (H 2 O 2 ) and hydroxyl ions [20]. Phagocytosis by monocytes/ macrophages is associated with a respiratory burst, the phagocytosing cells increase oxygen uptake and thereby form H 2 O 2 and O 2 2 radicals [21].…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen intermediates, nitrite and IFN-γin Indian visceral leishmaniasis

Kumar

Pai

Sundar

2001

Clinical and Experimental Immunology

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SUMMARY Reactive oxygen intermediates (ROI), nitrite and interferon-gamma (IFN-γ) production were investigated at different times during treatment in 10 patients with visceral leishmaniasis (VL). Hydrogen peroxide (H2O2), superoxide (O2−) and IFN-γ production by cultured monocytes from patients with active VL were significantly lower compared with the healthy controls. In contrast, nitrite levels in the supernatants from monocyte cultures of VL patients were comparable to healthy controls and increased significantly during antileishmanial therapy. On day 20 of treatment, a significant increase in the release of H2O2, O2− and IFN-γ was observed. However, at follow-up, 4 months after the end of treatment, the production of H2O2, O2−, IFN-γ and nitrite had declined significantly. Thus, the impairment in hydrogen peroxide and superoxide production suggests that down-regulation of these mediators may be involved in the reduced killing of parasites by monocytes of active VL patients. Furthermore, the monocytes regained respiratory burst activity as the antileishmanial therapy progressed, suggesting that an immune-based mechanism is involved in successful drug therapy.

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Section: Discussionmentioning

confidence: 99%

Reactive oxygen intermediates, nitrite and IFN-γin Indian visceral leishmaniasis

Kumar

Pai

Sundar

2001

Clinical and Experimental Immunology

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“…It is of considerable interest that this period coincides also with the time at which delayed basilar arterial lumi nal narrowing has previously been described (Del gado et aI., 1985). The finding of such an association may be of importance inasmuch as macrophage ac tivity and oxyhaemoglobin autooxidation are both well known to be associated with the generation and release of free radicals (Sutton et aI., 1976;Babior, 1978). Work by a number of authors has suggested that an excess of free radicals may be involved in the genesis of arterial wall damage and the angio graphically visible delayed cerebral arterial narrow ing that may follow SAH (Sakaki et aI., 1988;Steinke et aI., 1989;Zuccarello et aI., 1989).…”

Section: Discussionmentioning

confidence: 99%

The Time Course of Intracranial Pathophysiological Changes following Experimental Subarachnoid Haemorrhage in the Rat

Jackowski

Crockard

Burnstock

et al. 1990

J Cereb Blood Flow Metab

147

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Summary:The rat subarachnoid haemorrhage (SAH) model was further studied to establish the precise time course of the globally reduced CBF that follows and to ascertain whether temporally related changes in cerebral perfusion pressure (CPP) and intracranial pressure (lCP) take place. Parallel ultrastructural studies were per formed upon cerebral arteries and their adjacent perivas cular subarachnoid spaces. SAH was induced by a single intracisternal injection of autologous arterial blood. Serial measurements of regional cortical CBF by hydrogen clearance revealed that experimental SAH resulted in an immediate 50% global reduction in cortical flows that per sisted for up to 3 h post SAH. At 24 h, flows were still significantly reduced at 85% of control values (p < 0.05), but by 48 h had regained normal values and were main tained up to 5 days post SAH. ICP rose acutely after haemorrhage to nearly 50 mm Hg with C-type pressure waves being present. ICP then fell slowly, only fully re turning to control levels at 72 h. Acute hydrocephalus was observed on autopsy examination of SAH animals but not in controls. Reductions in CPP occurred post SAH, but only in the order of 15%, which could not alone account for the fall in CBF that took place. At 48 and, to a lesser extent, 24 h post SAH, myonecrosis confined largely to smooth muscle cells of the immediately sub in-

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“…Although NADPH oxidase-derived superoxide anion and its dismutation product hydrogen peroxide are the reactive oxygen species primarily formed, the concomitant release of myeloperoxidase results in the formation of hypochlorous acid as the major oxidant. Due to the high levels of reactive oxygen species occurring in the proximity of the sinusoidal endothelial and parenchymal cells, oxidative breakdown of the membrane PUFAs is one of the main molecular mechanisms of liver cell injury during reperfusion after ischemia [51][52][53][54] In addition to the generation of ROS, activated neutrophils release a number of proteases and hydrolytic enzymes by granule exocytosis, which may be directly cytotoxic to liver cells. It has been reported that serine proteases, such as elastase and cathepsine G, are mainly responsible for the injury [55][56][57].…”

Section: Neutrophil Activationmentioning

confidence: 99%

Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

Cutrn

Perrelli

Cavalieri

et al. 2002

Free Radical Biology and Medicine

151

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Abstract-Hepatic ischemia/reperfusion injury has immediate and deleterious effects on the outcome of patients after liver surgery. The precise mechanisms leading to the damage have not been completely elucidated. However, there is substantial evidence that the generation of oxygen free radicals and disturbances of the hepatic microcirculation are involved in this clinical syndrome. Microcirculatory dysfunction of the liver seems to be mediated by sinusoidal endothelial cell damage and by the imbalance of vasoconstrictor and vasodilator molecules, such as endothelin (ET), reactive oxygen species (ROS), and nitric oxide (NO). This may lead to no-reflow phenomenon with release of proinflammatory cytokines, sinusoidal plugging of neutrophils, oxidative stress, and as an ultimate consequence, hypoxic cell injury and parenchymal failure. An inducible potent endogenous mechanism against ischemia/reperfusion injury has been termed ischemic preconditioning. It has been suggested that preconditioning could inhibit the effects of different mediators involved in the microcirculatory dysfunction, including endothelin, tumor necrosis factor-␣, and oxygen free radicals. In this review, we address the mechanisms of liver microcirculatory dysfunction and how ischemic preconditioning could help to provide new surgical and/or pharmacological strategies to protect the liver against reperfusion damage.

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Oxygen-Dependent Microbial Killing by Phagocytes

Cited by 2,282 publications

References 81 publications

Reactive oxygen intermediates, nitrite and IFN-γin Indian visceral leishmaniasis

Reactive oxygen intermediates, nitrite and IFN-γin Indian visceral leishmaniasis

The Time Course of Intracranial Pathophysiological Changes following Experimental Subarachnoid Haemorrhage in the Rat

Microvascular dysfunction induced by reperfusion injury and protective effect of ischemic preconditioning

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