Monocyte‐derived macrophages as helper cells in monocyte‐mediated cytolysis

Dallegri, Franco; Ballestrero, Alberto; Frumento, Guido; Goretti, Riccardo; Patrone, Franco

doi:10.1111/j.1365-2141.1988.tb04175.x

Cited by 3 publications

(4 citation statements)

References 20 publications

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“…As well as being a potent microbicidal agent it is also implicated as a cause of neutrophil-mediated tissue injury [2,4]. Numerous studies have demonstrated its ability to damage cells [5][6][7] and extracellular matrix proteins [2,8,9], and to inactivate enzymes [10].…”

Section: Introductionmentioning

confidence: 99%

Oxidation of intracellular glutathione after exposure of human red blood cells to hypochlorous acid

Vissers

Winterbourn

1995

Biochemical Journal

122

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Exposure of human red blood cells to low doses of hypochlorous acid (HOCl) resulted in the loss of intracellular GSH. Oxidation occurred less than 2 min after the addition of HOCl, and required approx. 2.5 mol of HOCl per mol of GSH lost. Loss of GSH preceded oxidation of membrane thiols, the formation of chloramines and haemoglobin oxidation. The susceptibility of intracellular GSH to oxidation by HOCl was two-thirds that of GSH in cell lysates. These results indicate that HOCl can penetrate the red cell membrane, which provides little barrier protection for cytoplasmic components, and that GSH oxidation by HOCl may be a highly selective process. Virtually all of the GSH lost was converted into GSSG. If glucose was added to the medium, most of the GSH oxidized by low doses of HOCl was rapidly regenerated. At higher doses, recovery was less efficient. However, when HOCl was added as a slow infusion rather than in a single bolus, there was increased recovery at higher doses. This indicates that in metabolically active cells regeneration is rapid and GSH may protect cell components from damage by HOCl. HOCl-induced lysis was only slightly delayed by adding glucose to the medium, indicating that lytic injury is not ameliorated by GSH.

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Section: Introductionmentioning

confidence: 99%

Oxidation of intracellular glutathione after exposure of human red blood cells to hypochlorous acid

Vissers

Winterbourn

1995

Biochemical Journal

122

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“…We have shown that regeneration of thiols did not prevent HOCl-mediated red cell lysis [14], and it is not clear whether thiol oxidation results in irreversible cell injury. Other reactive groups are Fe-S centres [7], thiolate bonds in zinc proteins [16] adenine nucleotides [17,18], alkenes [19,20] and amino groups, producing chloramines that are also strong oxidants [1,13]. The reaction with unsaturated fatty acids and cholesterol results in the formation of chlorohydrins [19,21], which are potentially destabilizing to the cell membrane and might cause permeability changes.…”

Section: Introductionmentioning

confidence: 99%

“…Red blood cells have been used extensively as a model system for investigating mechanisms of neutrophil-mediated cell injury [11,12,14,17,26]. Haemolysis is dependent on HOCl and is not readily mediated by chloramines [11,17].…”

Section: Introductionmentioning

confidence: 99%

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Comparison of human red cell lysis by hypochlorous and hypobromous acids: insights into the mechanism of lysis

Vissers

Carr

Chapman

1998

Biochemical Journal

103

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Human red blood cells are lysed by the neutrophil-derived oxidant hypochlorous acid (HOCl), although the mechanism of lysis is unknown. Hypobromous acid (HOBr), a similarly reactive oxidant, lysed red cells approx. 10-fold faster than HOCl. Therefore we compared the effects of these oxidants on thiols, membrane lipids and proteins to determine which reactions are associated with lysis. There was no difference in the loss of reduced glutathione or membrane thiols with either oxidant, but HOBr reacted more readily with membrane lipids and proteins. Bromohydrin derivatives of phospholipids and cholesterol were seen at approx. one-tenth the level of oxidant than chlorohydrins were. However, these products were detected only with high concentrations of HOCl or HOBr, which caused instant haemolysis. Membrane protein modification occurred at much lower doses of oxidant and was more closely correlated with lysis. SDS/PAGE analysis showed that band 3, the anion transport protein, was lost at the lowest dose of HOBr and at the higher concentrations of HOCl. Labelling the red cells with eosin 5-maleimide, a fluorescent label for band 3, suggested possible clustering of this protein in oxidant-exposed cells. There was also irreversible cross-linking of all the major membrane proteins; this reaction occurred more readily with HOBr. The results indicate that membrane protein modification is the reaction responsible for HOCl-mediated lysis. These effects, and particularly cross-link formation, might result in clustering of band 3 and other membrane and cytoskeletal proteins to form haemolytic pores.

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Effect of leukopenia on experimental post-traumatic retinal detachment

Gabrielian

Wang

Lee

et al. 1994

Current Eye Research

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Macrophages are invariably present in the intraocular membranes of patients with traumatic proliferative vitreoretinopathy (PVR). There are two sources from which these macrophages could be recruited: adjacent tissues and the systemic circulation. In the study described herein, the role of circulating white blood cells and monocytes in experimental, traumatic PVR was studied. The circulating white blood cells of 20 rabbits were depleted by intravenous injection of strontium-89. Posterior perforating eye injury with subsequent intravitreal injection of autologous whole blood or autologous activated macrophages was then performed on these leukopenic animals. The experiments demonstrated that severe bone marrow depression reduced significantly the incidence of retinal detachments in eyes receiving whole blood, and reduced the severity of retinal detachments in eyes injected with activated macrophages. An association between the degree of leukopenia, monocytopenia, and protection from retinal detachment was demonstrated. These results support the hypothesis that macrophage infiltration is an important component of intraocular cellular proliferation, but does not exclude the role of other types of white blood cells in the pathogenesis of PVR.

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Monocyte‐derived macrophages as helper cells in monocyte‐mediated cytolysis

Cited by 3 publications

References 20 publications

Oxidation of intracellular glutathione after exposure of human red blood cells to hypochlorous acid

Oxidation of intracellular glutathione after exposure of human red blood cells to hypochlorous acid

Comparison of human red cell lysis by hypochlorous and hypobromous acids: insights into the mechanism of lysis

Effect of leukopenia on experimental post-traumatic retinal detachment

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