Human neutrophil (PMN) oxygen radical production and the cytoskeleton

Wiles, Marc E.; Dykens, James A.; Wright, Clifford D.

doi:10.1016/0024-3205(95)02114-x

Cited by 20 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Others have observed that FMLP stimulation of respiratory burst response is up-regulated when cells are pretreated with an inhibitor of actin assembly, cytochalasin D (39,40). These observations suggest that ERK-mediated actin assembly regulates respiratory burst activity.…”

Section: Discussionmentioning

confidence: 87%

“…Alternative mechanisms may exist for regulation of the Fc␥RIIa-and Fc␥RIIIb-mediated respiratory burst response. Previous reports indicate that actin associates with components of the NADPH-oxidase complex such as p47 phox , p76 phox , and cytochrome b 558 (38,39). Thus, another possible mechanism by which actin polymerization regulates respiratory burst activity may be through inhibition of assembly of the NADPH oxidase enzyme complex.…”

Section: Discussionmentioning

confidence: 99%

“…Past studies have shown that inhibition of actin polymerization enhances FMLP stimulation of respiratory burst activity (39,40), suggesting that actin reorganization can regulate this response. The present study shows that inhibition of ERK activity blocks Fc␥R stimulation of actin polymerization, while enhancing Fc␥R stimulation of respiratory burst activity (see Figs.…”

Section: Effect Of Actin Polymerization On Fc␥r-stimulated Mapk Activmentioning

confidence: 98%

See 2 more Smart Citations

Differential Mitogen-Activated Protein Kinase Stimulation by Fcγ Receptor IIa and Fcγ Receptor IIIb Determines the Activation Phenotype of Human Neutrophils

Coxon¹,

Rane²,

Powell

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

FcγRs mediate immune complex-induced tissue injury. The hypothesis that FcγRIIa and FcγRIIIb control neutrophil responses by activating mitogen-activated protein kinases was examined. Homotypic and heterotypic cross-linking of FcγRIIa and/or FcγRIIIb resulted in a rapid, transient increase in ERK and p38 activity, with maximal stimulation between 1 and 3 min. FcγRIIa and FcγRIIIb stimulated distinct patterns of ERK and p38 activity, and heterotypic cross-linking failed to stimulate synergistic activation of either ERK or p38 activity. Both FcγRIIa and FcγRIIIb required activation of a nonreceptor tyrosine kinase and phosphatidylinositol 3-kinase for stimulation of ERK and p38. Inhibition of ERK activation with PD98059 enhanced H2O2 production stimulated by homotypic and heterotypic FcγR cross-linking. Inhibition of p38 with SB203580 attenuated H2O2 production stimulated by FcγRIIIb or heterotypic cross-linking, but had no effect on FcγRIIa-stimulated H2O2 production. On the other hand, PD98059 inhibited actin polymerization stimulated by FcγR cross-linking, while SB203580 had no effect. Inhibition of actin polymerization with cytochalasin D enhanced p38 activity stimulated by either FcγRIIa or FcγRIIIb, but cytochalasin D only enhanced H2O2 production stimulated by FcγRIIIb. Our data indicate that FcγRIIa and FcγRIIIb independently activate ERK and p38. The two receptors demonstrate different efficacies for ERK and p38 activation, and they do not act cooperatively. ERK and p38 provide stimulatory and inhibitory signals for neutrophil responses to immune complexes. In addition, these data indicate that actin reorganization may play a role in mediating p38-dependent activation of respiratory burst upon stimulation of FcγRIIIb in neutrophils.

show abstract

Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Effect Of Actin Polymerization On Fc␥r-stimulated Mapk Activmentioning

confidence: 98%

See 1 more Smart Citation

Differential Mitogen-Activated Protein Kinase Stimulation by Fcγ Receptor IIa and Fcγ Receptor IIIb Determines the Activation Phenotype of Human Neutrophils

Coxon¹,

Rane²,

Powell

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…Changes in the average length of actin filaments are required for the migration and activation of the respiratory burst of granulocytes [24,25]. In eosinophils actin filaments are dynamic and undergo self-assembly and disassembly in response to chemokines such as eotaxin, RANTES, MCP-3 and MCP-4 [20,23].…”

Section: Eotaxin-2 Induced Actin Polymerization In Human Eosinophilsmentioning

confidence: 99%

Eotaxin-2 activates chemotaxis-related events and release of reactive oxygen species via pertussis toxin-sensitive G proteins in human eosinophils

et al. 1998

View full text Add to dashboard Cite

Eosinophils play an important role in allergic and autoimmune diseases. They are activated by distinct chemokines, leading to the immigration into the inflamed tissue, and mediate tissue damage by releasing reactive oxygen species. Recently, eotaxin was found to have the broadest spectrum of activities of all eosinophil-activating CC chemokines. In this study we investigated the effect of the novel CC chemokine, eotaxin-2, on eosinophil effector functions and compared its activity with eotaxin. Using nitrobenzoxadiazole-phallacidin staining and flow cytometry, we show that eotaxin-2 induced rapid and transient actin polymerization, a prerequisite for cell migration and modulation of the respiratory burst, in eosinophils in the same range of efficacy as observed for eotaxin. Eotaxin-2 induced the release of reactive oxygen species in a dose-dependent manner; half maximal and maximal release were found at 50 ng/ml and 500 ng/ml, respectively. Surprisingly, the efficacy of eotaxin-2 was comparable to that of eotaxin and C5a. Release of reactive oxygen species was inhibited by pertussis toxin, indicating the involvement of G i proteins in the signaling of eotaxin-2. Moreover, the anti-CC chemokine receptor 3 (CCR3) monoclonal antibody, 7B11, was able to inhibit transient rise in the cytosolic Ca 2+ concentration and the release of reactive oxygen species following stimulation with eotaxin-2. Therefore, eotaxin-2 represents a potent CC chemokine for human eosinophils activating chemotaxis-related events, such as actin polymerization, and the respiratory burst via the CCR3. Moreover, the efficacy of eotaxin-2 seems to be in the same range as that of eotaxin which might re-evaluate the recent profile of activity of CC chemokines in the activation of human eosinophils.

show abstract

“…5). Cytochalasin b enhances FMLPinduced ROS production by inhibiting F-actin formation and subsequent internalization and inactivation of FMLP-receptors (Wiles et al, 1995;Vocks et al, 2003). The similarities between the effects of cytochalasin b and CNI-1493 on F-actin polymerization could explain the increased ROS production in FMLP activated granulocytes in the presence of CNI-1493.…”

Section: Discussionmentioning

confidence: 87%