scholarly journals Involvement of Reactive Oxygen Intermediates in Spontaneous and CD95(Fas/APO-1)–Mediated Apoptosis of Neutrophils

Blood ◽  
1997 ◽  
Vol 89 (5) ◽  
pp. 1748-1753 ◽  
Author(s):  
Yoshihito Kasahara ◽  
Kazuyuki Iwai ◽  
Akihiro Yachie ◽  
Kunio Ohta ◽  
Akihiro Konno ◽  
...  
Keyword(s):  
Signal Transduction Pathway ◽  
Reactive Oxygen ◽  
Reactive Oxygen Intermediates ◽  
Transduction Pathway ◽  
Spontaneous Apoptosis ◽  
Oxygen Intermediates ◽  
Hereditary Defect ◽  
Oxidative Products

Apoptosis is well known to be mediated by oxidative stress. To evaluate the functional role of reactive oxygen intermediates (ROI) produced by neutrophils, we compared the rates of apoptosis in neutrophils isolated from normal donors and from patients with chronic granulomatous disease (CGD), a hereditary defect in ROI production. Spontaneous cell death in CGD neutrophils in vitro was significantly inhibited relative to normal neutrophils. The acceleration of apoptosis induced by anti-Fas monoclonal antibody (MoAb) in CGD neutrophils was much slower than that seen in normal neutrophils. These findings suggest that the apoptosis of neutrophils may be mediated by endogenous oxidative products. This suggestion was confirmed by observation that apoptosis of normal neutrophils was markedly inhibited by reduction of intracellular levels of hydrogen peroxide (H2O2 ). The inhibition of apoptosis in normal neutrophils by adding catalase occurred regardless of the presence of anti-Fas MoAb. H2O2 increased both spontaneous apoptosis and Fas-mediated apoptosis of the CGD neutrophils in proportion to that seen in normal neutrophils. Although several factors that mediate the apoptosis of neutrophils remain to be determined, these results suggest that ROI are major mediators of the apoptosis in neutrophils and may be involved in Fas-mediated signal transduction pathway.

scholarly journals Involvement of Reactive Oxygen Intermediates in Spontaneous and CD95(Fas/APO-1)–Mediated Apoptosis of Neutrophils

Blood ◽  
1997 ◽  
Vol 89 (5) ◽  
pp. 1748-1753 ◽  
Author(s):  
Yoshihito Kasahara ◽  
Kazuyuki Iwai ◽  
Akihiro Yachie ◽  
Kunio Ohta ◽  
Akihiro Konno ◽  
...  
Keyword(s):  
Signal Transduction Pathway ◽  
Reactive Oxygen ◽  
Reactive Oxygen Intermediates ◽  
Transduction Pathway ◽  
Spontaneous Apoptosis ◽  
Oxygen Intermediates ◽  
Hereditary Defect ◽  
Oxidative Products

Abstract Apoptosis is well known to be mediated by oxidative stress. To evaluate the functional role of reactive oxygen intermediates (ROI) produced by neutrophils, we compared the rates of apoptosis in neutrophils isolated from normal donors and from patients with chronic granulomatous disease (CGD), a hereditary defect in ROI production. Spontaneous cell death in CGD neutrophils in vitro was significantly inhibited relative to normal neutrophils. The acceleration of apoptosis induced by anti-Fas monoclonal antibody (MoAb) in CGD neutrophils was much slower than that seen in normal neutrophils. These findings suggest that the apoptosis of neutrophils may be mediated by endogenous oxidative products. This suggestion was confirmed by observation that apoptosis of normal neutrophils was markedly inhibited by reduction of intracellular levels of hydrogen peroxide (H2O2 ). The inhibition of apoptosis in normal neutrophils by adding catalase occurred regardless of the presence of anti-Fas MoAb. H2O2 increased both spontaneous apoptosis and Fas-mediated apoptosis of the CGD neutrophils in proportion to that seen in normal neutrophils. Although several factors that mediate the apoptosis of neutrophils remain to be determined, these results suggest that ROI are major mediators of the apoptosis in neutrophils and may be involved in Fas-mediated signal transduction pathway.

scholarly journals Role of Reactive Oxygen Intermediates in Cellular Responses to Dietary Cancer Chemopreventive Agents

Planta Medica ◽  
2008 ◽  
Vol 74 (13) ◽  
pp. 1570-1579 ◽  
Author(s):  
Jedrzej Antosiewicz ◽  
Wieslaw Ziolkowski ◽  
Siddhartha Kar ◽  
Anna Powolny ◽  
Shivendra Singh
Keyword(s):  
Reactive Oxygen ◽  
Cellular Responses ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates ◽  
Chemopreventive Agents

scholarly journals Coxiella burnetiiAcid Phosphatase Inhibits the Release of Reactive Oxygen Intermediates in Polymorphonuclear Leukocytes

2010 ◽  
Vol 79 (1) ◽  
pp. 414-420 ◽  
Author(s):  
J. Hill ◽  
J. E. Samuel
Keyword(s):  
Acid Phosphatase ◽  
Nadph Oxidase ◽  
Polymorphonuclear Leukocytes ◽  
Q Fever ◽  
Reactive Oxygen ◽  
Host Cells ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates

ABSTRACTCoxiella burnetii, the etiological agent of Q fever, is a small, Gram-negative, obligate intracellular bacterium. Replication ofC. burnetiiduring infection has been shown to be increased by decreasing oxidative stress using p47phox −/−and iNOS−/−micein vivoand by pharmacologic inhibitorsin vitro. Building upon this model, we investigated the role polymorphonuclear leukocytes (PMN) play in the control of infection, since NADPH oxidase-mediated release of reactive oxygen intermediates (ROI) is a primary bactericidal mechanism for these cells that is critical for early innate clearance. Earlier studies suggested thatC. burnetiiactively inhibited release of ROI from PMN through expression of an unidentified acid phosphatase (ACP). Recent genomic annotations identified one open reading frame (CBU0335) which may encode a Sec- and type II-dependent secreted ACP. To test this model, viableC. burnetiipropagated in tissue culture host cells or axenic media,C. burnetiiextracts, or purified recombinant ACP (rACP) was combined with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA). The release of ROI was inhibited when PMN were challenged with viableC. burnetii,C. burnetiiextracts, or rACP but not when PMN were challenged with electron beam-inactivatedC. burnetii. C. burnetiiextracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN membranes, suggesting a molecular mechanism responsible for this inhibition. These data support a model in whichC. burnetiieludes the primary ROI killing mechanism of activated PMN by secreting at least one acid phosphatase.

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