Superoxide generation by digitonin-stimulated guinea pig granulocytes. A basis for a continuous assay for monitoring superoxide production and for the study of the activation of the generating system.

Cohen, Harvey J.; Chovaniec, Margaret E.

doi:10.1172/jci109007

Cited by 405 publications

(93 citation statements)

References 22 publications

(29 reference statements)

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“…Our findings that no significant generation of such radicals took place when PMNs had been treated with large amounts of LTA alone suggests that not every agent which binds to PMN membranes elicits a respiratory burst. Thus, LTA differs from other membraneperturbing agents, e.g., lectins (65), FMLP peptides (66,67), saponin (68), digitonin (68), lysolecithin (69), cationic poly-amino acids (49,52,55,56), lipopolysaccharides (58), etc., which bind to PMN and macrophage membranes and elicit a respiratory burst. To secure the generation of O~-and chemiluminescence (CL), LTA-sensitized PMNs must be further treated with anti-LTA antibodies (Figures 1-7).…”

Section: Discussionmentioning

confidence: 99%

Lipoteichoic acid-antilipoteichoic acid complexes induce superoxide generation by human neutrophils

et al. 1988

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Abstract--Human neutrophils (PMNs) which have been incubated with lipoteichoic acid (LTA) from group A streptococci generated large amounts of superoxide (O~-chemiluminescence and hydrogen peroxide when challenged with anti-LTA antibodies. Cytochalasin B further enhanced Oy generation. The onset of O2 generation by the LTA-anti-LTA complexes was much faster than that induced by BSA-anti-BSA complexes. LTA-treated PMNs generated much less 02 when challenged with BSA complexes, suggesting that LTA might have blocked, nonspecifically, some of the Fe receptors on PMNs. PMNs treated with LTA-anti-LTA complexes further interacted with bystander nonsensitized PMNs resulting in enhanced O~-generation, suggesting that small numbers of LTA-sensitized PMNs might recruit additional PMNs to participate in the generation of toxic oxygen species. Protelolytic enzyme treatment of PMNs further enhanced the generation of 02 by PMNs treated with LTAanti-LTA. Superoxide generation could also be induced when PMNs and anti-LTA antibodies interacted with target cells (fibroblasts, epithelial cells) pretreated with LTA. This effect was also further enhanced by pretreatment of the target cells with proteases. PMNs incubated with LTA released lysosomal enzymes following treatment with anti-LTA antibodies. The amounts of phosphatase, /3-glucoronidase, Nacetylglucosaminidase, mannosidase, and lysozyme release by LTA-anti-LTA complexes were much smaller than those released by antibody or histone-opsonized streptococci, suggesting that opsonized particles are more efficient lysosomal enzyme releasers. However, since the amounts of O~-generated by the LTA complexes equaled those generated by the opsonized particles, it is assumed that the signals for triggering a respiratory burst and lysosomal enzyme secretion might be different.

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Section: Discussionmentioning

confidence: 99%

Lipoteichoic acid-antilipoteichoic acid complexes induce superoxide generation by human neutrophils

et al. 1988

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“…Superoxide release was measured by following the superoxide dismutaseinhibitable reduction of ferricytochrome c at 550 nm [21].…”

Section: Secretion Assaysmentioning

confidence: 99%

Neutrophil degranulation and phospholipase D activation are enhanced if the Na+/H+ antiport is blocked

Gewirtz

Seetoo

Simons

1998

Journal of Leukocyte Biology

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To investigate the role of the pH transient in controlling degranulation, the Na ؉ /H ؉ antiport was inhibited either with 100 M dimethylamiloride (DMA) or by substituting N-methyl-glucamine for extracellular sodium. Blocking the antiport with DMA led to hyperacidified PMN, which exhibited an increase in degranulation, but did not affect generation of superoxide. DMA did not alter the ability of neutrophils to phagocytose and oxidize dichlorodihydrofluoresceinated HIC, suggesting the increase in degranulation was not the result of failed phagocytosis. Investigation into whether the observed increase in degranulation when the antiport was blocked was mediated by PLD or ⌬[Ca 2؉ ] in revealed that blocking the antiport increased HICinduced PLD activity but had no effect on HICinduced ⌬[Ca 2؉ ] in . Blocking the Na ؉ /H ؉ antiport by ion substitution caused similar effects on PMN signaling and secretion as was seen with DMA. These results indicate that Na ؉ /H ؉ antiport activity is not necessary for degranulation or superoxide release in HICstimulated PMN and that hyperacidification of the cytoplasm can modulate degranulation. Therefore, pH in , via its effect on PLD, may be a control point of degranulation and may represent one way that neutrophils achieve differential control of their antibacterial products. J. Leukoc. Biol. 64: 98-103; 1998.

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“…O 2 Ϫ release was measured by the SOD-inhibitable reduction of ferricytochrome c, as quantitated by the increase in absorbance at 550 nM [19]. Freshly isolated PMN were suspended in HBSS at a final cell density of 2 ϫ 10 6 /mL.…”

Section: Measurement Of O 2 ϫ Releasementioning

confidence: 99%

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

Kausalya

Nath

1998

Journal of Leukocyte Biology

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Superoxide generation by digitonin-stimulated guinea pig granulocytes. A basis for a continuous assay for monitoring superoxide production and for the study of the activation of the generating system.

Cited by 405 publications

References 22 publications

Lipoteichoic acid-antilipoteichoic acid complexes induce superoxide generation by human neutrophils

Lipoteichoic acid-antilipoteichoic acid complexes induce superoxide generation by human neutrophils

Neutrophil degranulation and phospholipase D activation are enhanced if the Na+/H+ antiport is blocked

Interactive role of nitric oxide and superoxide anion in neutrophil-mediated endothelial cell injury

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