Endotoxemia and Oxidative Stressa

Pattanaik, Uttara; Prasad, Kailash

doi:10.1111/j.1749-6632.1996.tb33551.x

Cited by 15 publications

(12 citation statements)

References 12 publications

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“…One mechanism by which LPS mediates inflammatory effect is to increase the cellular oxidative stress (60), which has been known to be very harmful to hemopoietic cells particularly to those from Fanconi patients (1). We suspected that TNF-␣-induced ROS was the source of LPS-generated cellular oxidative stress responsible in part for the observed hemopoietic suppression.…”

Section: The Role Of Tnf-␣-induced Ros In Hemopoietic Suppression By Lpsmentioning

confidence: 99%

Inflammatory Reactive Oxygen Species-Mediated Hemopoietic Suppression in Fancc-Deficient Mice

Sejas

Rani

Qiu

et al. 2007

The Journal of Immunology

102

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Patients with the genomic instability syndrome Fanconi anemia (FA) commonly develop progressive bone marrow (BM) failure and have a high risk of cancer. Certain manifestations of the disease suggest that the FA immune system is dysfunctional and may contribute to the pathogenesis of both BM failure and malignancies. In this study, we have investigated inflammation and innate immunity in FA hemopoietic cells using mice deficient in Fanconi complementation group C gene (Fancc). We demonstrate that Fancc-deficient mice exhibit enhanced inflammatory response and are hypersensitive to LPS-induced septic shock as a result of hemopoietic suppression. This exacerbated inflammatory phenotype is intrinsic to the hemopoietic system and can be corrected by the re-expression of a wild-type FANCC gene, suggesting a potential role of the FANCC protein in innate immunity. LPS-mediated hemopoietic suppression requires two major inflammatory agents, TNF-α and reactive oxygen species. In addition, LPS-induced excessive accumulation of reactive oxygen species in Fancc−/− BM cells overactivates the stress kinase p38 and requires prolonged activation of the JNK. Our data implicate a role of inflammation in pathogenesis of FA and BM failure diseases in general.

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Section: The Role Of Tnf-␣-induced Ros In Hemopoietic Suppression By Lpsmentioning

confidence: 99%

Inflammatory Reactive Oxygen Species-Mediated Hemopoietic Suppression in Fancc-Deficient Mice

Sejas

Rani

Qiu

et al. 2007

The Journal of Immunology

102

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“…LPS has been shown to cause an increase in cellular oxidative stress (31). However, whether this increase in ROS reflects a direct response to LPS or an indirect response to LPS-induced cytokine release remains controversial (31).…”

Section: Ros Generation During Lps Is Dependent On the Production Of mentioning

confidence: 99%

“…However, whether this increase in ROS reflects a direct response to LPS or an indirect response to LPS-induced cytokine release remains controversial (31). To assess whether LPS directly induces generation of ROS, murine macrophage J774.1 cells were placed in a flowthrough chamber on an inverted microscope under normoxic conditions (15% O 2 ) in the presence of LPS (1 g/ml) and DCFH-DA (10 M) for 90 min.…”

Section: Ros Generation During Lps Is Dependent On the Production Of mentioning

confidence: 99%

Role of Oxidants in NF-κB Activation and TNF-α Gene Transcription Induced by Hypoxia and Endotoxin

Chandel

Trzyna

McClintock

et al. 2000

The Journal of Immunology

486

281

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The transcription factor NF-κB stimulates the transcription of proinflammatory cytokines including TNF-α. LPS (endotoxin) and hypoxia both induce NF-κB activation and TNF-α gene transcription. Furthermore, hypoxia augments LPS induction of TNF-α mRNA. Previous reports have indicated that antioxidants abolish NF-κB activation in response to LPS or hypoxia, which suggests that reactive oxygen species (ROS) are involved in NF-κB activation. This study tested whether mitochondrial ROS are required for both NF-κB activation and the increase in TNF-α mRNA levels during hypoxia and LPS. Our results indicate that hypoxia (1.5% O2) stimulates NF-κB and TNF-α gene transcription and increases ROS generation as measured by the oxidant sensitive dye 2′,7′-dichlorofluorescein diacetate in murine macrophage J774.1 cells. The antioxidants N-acetylcysteine and pyrrolidinedithiocarbamic acid abolished the hypoxic activation of NF-κB, TNF-α gene transcription, and increases in ROS levels. Rotenone, an inhibitor of mitochondrial complex I, abolished the increase in ROS signal, the activation of NF-κB, and TNF-α gene transcription during hypoxia. LPS stimulated NF-κB and TNF-α gene transcription but not ROS generation in J774.1 cells. Rotenone, pyrrolidinedithiocarbamic acid, and N-acetylcysteine had no effect on the LPS stimulation of NF-κB and TNF-α gene transcription, indicating that LPS activates NF-κB and TNF-α gene transcription through a ROS-independent mechanism. These results indicate that mitochondrial ROS are required for the hypoxic activation of NF-κB and TNF-α gene transcription, but not for the LPS activation of NF-κB.

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“…causes a significant increase in cellular oxidative stress (44) and these reactive oxygen species play an important role in activation of NFB. We observed that melittin neutralized LPS-induced reactive oxygen species generation, whereas its analogue MM-1 was found to partially neutralize oxidative stress but MM-2 and Mel-SCR almost completely failed to inhibit ROS augmentation in these LPS-stimulated cells (supplemental Fig.…”

Section: State Of Lps-stimulated Oxidative Stress With Treatment Of Mmentioning

confidence: 99%

Consequences of Alteration in Leucine Zipper Sequence of Melittin in Its Neutralization of Lipopolysaccharide-induced Proinflammatory Response in Macrophage Cells and Interaction with Lipopolysaccharide

Srivastava

Srivastava²,

Singh

et al. 2012

Journal of Biological Chemistry

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Background: Bee venom antimicrobial peptide, melittin, neutralizes LPS-induced proinflammatory response in macrophage cells. Results: Alteration in the leucine zipper sequence of melittin impaired its anti-LPS property and interaction with LPS. Conclusion:The leucine zipper sequence of melittin plays a crucial role in maintaining its antiendotoxin properties. Significances:The results suggest an overlap of structural requirements for the cytotoxic and antiendotoxin properties of melittin.

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Endotoxemia and Oxidative Stressa

Cited by 15 publications

References 12 publications

Inflammatory Reactive Oxygen Species-Mediated Hemopoietic Suppression in Fancc-Deficient Mice

Inflammatory Reactive Oxygen Species-Mediated Hemopoietic Suppression in Fancc-Deficient Mice

Role of Oxidants in NF-κB Activation and TNF-α Gene Transcription Induced by Hypoxia and Endotoxin

Consequences of Alteration in Leucine Zipper Sequence of Melittin in Its Neutralization of Lipopolysaccharide-induced Proinflammatory Response in Macrophage Cells and Interaction with Lipopolysaccharide

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