Regulation of cytokine gene expression by reactive oxygen and reactive nitrogen intermediates

Remick, Daniel G.; Villarete, Lorelie

doi:10.1002/jlb.59.4.471

Cited by 131 publications

(58 citation statements)

References 27 publications

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“…gp91 phox2/-mice had increased production of proinflammatory cytokines and chemokines and these will also have modified neutrophil phenotype indirectly. The sustained production of CXC chemokines is noteworthy because inhibition of ROS signaling by antioxidants has previously been associated with down-regulation of CXC chemokine expression (34), suggesting in our model a shift to ROS-independent chemokine expression. The neutrophil activation status reflects the proinflammatory cytokine environment and the up-regulation of b 2 -integrin, which, in the absence of ROS generation (35), stimulates prosurvival pathways (36).…”

Section: Discussionmentioning

confidence: 56%

Reactive Oxygen Species Regulate Neutrophil Recruitment and Survival in Pneumococcal Pneumonia

Marriott

Jackson

Wilkinson³

et al. 2008

Am J Respir Crit Care Med

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Rationale: The role of NADPH oxidase activation in pneumonia is complex because reactive oxygen species contribute to both microbial killing and regulation of the acute pulmonary infiltrate. The relative importance of each role remains poorly defined in communityacquired pneumonia. Objectives: We evaluated the contribution of NADPH oxidasederived reactive oxygen species to the pathogenesis of pneumococcal pneumonia, addressing both the contribution to microbial killing and regulation of the inflammatory response. Methods: Mice deficient in the gp91 phox component of the phagocyte NADPH oxidase were studied after pneumococcal challenge. Measurements and Main Results: gp91 phox2/-mice demonstrated no defect in microbial clearance as compared with wild-type C57BL/6 mice. A significant increase in bacterial clearance from the lungs of gp91 phox2/-mice was associated with increased numbers of neutrophils in the lung, lower rates of neutrophil apoptosis, and enhanced activation. Marked alterations in pulmonary cytokine/ chemokine expression were also noted in the lungs of gp91 phox2/-mice, characterized by elevated levels of tumor necrosis factor-a, KC, macrophage inflammatory protein-2, monocyte chemotactic protein-1, and IL-6. The greater numbers of neutrophils in gp91 phox2/-mice were not associated with increased lung injury. Levels of neutrophil elastase in bronchoalveolar lavage were not decreased in gp91 phox2/-mice. Conclusions: During pneumococcal pneumonia, NADPH oxidasederived reactive oxygen species are redundant for host defense but limit neutrophil recruitment and survival. Decreased NADPH oxidasedependent reactive oxygen species production is well tolerated and improves disease outcome during pneumococcal pneumonia by removing neutrophils from the tight constraints of reactive oxygen species-mediated regulation.

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Section: Discussionmentioning

confidence: 56%

Reactive Oxygen Species Regulate Neutrophil Recruitment and Survival in Pneumococcal Pneumonia

Marriott

Jackson

Wilkinson³

et al. 2008

Am J Respir Crit Care Med

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“…The relationship between oxidants and cytokines is complex. Oxidants both stimulated the production of cytokines (55,56) and mediated effects of cytokines (57). Both oxidants and cytokines were reported to signal through protein kinase C isoforms (56, 58 -60).…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Activates the Plasminogen Activator Inhibitor Type 1 (PAI-1) Promoter through an AP-1 Response Element and Cooperates with Insulin for Additive Effects on PAI-1 Transcription

Vulin

Stanley

2004

Journal of Biological Chemistry

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Oxidative stress is one of the characteristics of diabetes and is thought to be responsible for many of the pathophysiological changes caused by the disease. We previously identified an insulin response element in the promoter of plasminogen activator inhibitor 1 (PAI-1) that was activated by an unidentified member of the forkhead/winged helix (Fox) family of transcription factors. This element mediated a 5-7-fold increase in PAI-1 transcription because of insulin. Here we report that oxidative stress also caused a 3-fold increase in PAI-1 transcription and that the effect was additive with that of insulin. Antioxidants prevent this response. Mutational analysis of the PAI-1 promoter revealed that oxidative stress acted at an AP-1 site at ؊60/52 of the promoter. Gel mobility shift analysis demonstrated that binding to an AP-1 oligonucleotide was increased 4-fold by oxidative stress. Jun levels were increased by oxidants as assessed by reverse transcriptase-PCR. Western blotting demonstrated that a rapid and prolonged nuclear accumulation of phospho-c-Jun followed oxidant stimulation. The nuclear c-Jun phosphorylation was not observed in cells treated with reduced glutathione. Finally, JNK/SAPK activity was found to increase in response to oxidants, and inhibition of JNK/SAP blocked TBHQ-increased PAI-1-luciferase expression. Thus, oxidative stress stimulated AP-1 and activated the PAI-1 promoter.

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“…I/ R injury induces an inflammatory response, which results in the formation of reactive oxygen species (ROS) that augments local tissue damage or affects organs remote from the site of I/R. An important function of ROS is the regulation of cytokine gene expression [3] .…”

Section: Introductionmentioning

confidence: 99%

Effects of different periods of renal ischemia on liver as a remote organ

Kadkhodaee

Golab²,

Zahmatkesh³

et al. 2009

WJG

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AIM:To assess the hepatic changes after induction of different periods of renal ischemia. METHODS:Rats were subjected to either sham operation or ischemia (30, 45 and 60 min) followed by 60 min reperfusion. Liver and renal functional indices were measured. Hepatic glutathione (GSH) and ferric reducing antioxidant power levels and the concentration of interleukin (IL)-10 and tumor necrosis factor (TNF-α) were evaluated. Portions of liver and kidney tissues were fixed for histological evaluation. RESULTS:Forty-five minutes renal ischemia followed by 60 min reperfusion caused significant changes in liver structure and a significant reduction in renal function. These rats showed a significant decrease in liver GSH, as well as a significant increase in TNF-α and IL-10 concentrations. These results demonstrated that renal ischemia caused changes in liver histology, function, oxidative stress and inflammatory status, which led to a reduction in hepatic antioxidant capacity. With 30 min ischemia, the magnitude of these changes was less than those with 45 or 60 min ischemia. CONCLUSION:A minimum of 45 min ischemia is needed to study the effects of renal injury on the liver as a remote organ.

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Regulation of cytokine gene expression by reactive oxygen and reactive nitrogen intermediates

Cited by 131 publications

References 27 publications

Reactive Oxygen Species Regulate Neutrophil Recruitment and Survival in Pneumococcal Pneumonia

Reactive Oxygen Species Regulate Neutrophil Recruitment and Survival in Pneumococcal Pneumonia

Oxidative Stress Activates the Plasminogen Activator Inhibitor Type 1 (PAI-1) Promoter through an AP-1 Response Element and Cooperates with Insulin for Additive Effects on PAI-1 Transcription

Effects of different periods of renal ischemia on liver as a remote organ

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