Endotoxin-induced organ injury

Ghosh, Sunit; Latimer, R.D.; Gray, Beverly M.; Harwood, Robert; Oduro, A.

doi:10.1097/00003246-199302001-00005

Cited by 106 publications

(57 citation statements)

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“…LPS released from the outer membrane of gram-negative bacteria triggers leukocytes to synthesize and release a cascade of inflammatory mediators that ultimately can lead to tissue injury and multiple organ failure. 22 Multiple cells from the immune system are involved in this process. The hyperresponsiveness of Abca1-deficient mice to inflammation was demonstrated when Abca1-deficient mice were administered intraperitoneal injections of LPS at various doses.…”

Section: Lps-induced Septic Shock Is Exacerbated In Abca1-deficient Micementioning

confidence: 99%

Increased Cholesterol Deposition, Expression of Scavenger Receptors, and Response to Chemotactic Factors in Abca1 -Deficient Macrophages

Francone

Royer

Boucher

et al. 2005

ATVB

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Section: Lps-induced Septic Shock Is Exacerbated In Abca1-deficient Micementioning

confidence: 99%

Increased Cholesterol Deposition, Expression of Scavenger Receptors, and Response to Chemotactic Factors in Abca1 -Deficient Macrophages

Francone

Royer

Boucher

et al. 2005

ATVB

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“…1 Systemic exposure to LPS also initiates a rapid recruitment of neutrophils and monocytes into specific host tissues. 20 The influx of inflammatory cells into tissues is coordinated by the expression of chemoattractants, such as monocyte chemoattractant protein (MCP-1), and adhesion molecules, such as intercellular adhesion molecule 1 (ICAM-1). [21][22][23] Importantly, ICAM-1 Ϫ/Ϫ mice are resistant to the lethal effects of LPS.…”

Section: Introductionmentioning

confidence: 99%

Regulation of tissue factor and inflammatory mediators by Egr-1 in a mouse endotoxemia model

Pawliński

Pedersen

Kehrle

et al. 2003

Blood

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In septic shock, tissue factor (TF) activates blood coagulation, and cytokines and chemokines orchestrate an inflammatory response. In this study, the role of Egr-1 in lipopolysaccharide (LPS) induction of TF and inflammatory mediators in vivo was evaluated using Egr-1 ؉/؉ and Egr-1 ؊/؊ mice. Administration of LPS transiently increased the steady-state levels of Egr-1 mRNA in the kidneys and lungs of Egr-1 ؉/؉ mice with maximal induction at one hour. Egr-1 was expressed in epithelial cells in the kidneys and lungs in untreated and LPS-treated mice. LPS induction of monocyte chemoattractant protein mRNA in the kidneys and lungs of Egr-1 ؊/؊ mice was not affected at 3 hours, but its expression was significantly reduced at 8 hours compared with the expression observed in Egr-1 ؉/؉ mice. Similarly, LPS induction of TF mRNA expression in the kidneys and lungs at 8 hours was reduced in Egr-1 ؊/؊ mice. However, Egr-1 deficiency did not affect plasma levels of tumor necrosis factor ␣ in endotoxemic mice. Moreover, Egr-1 ؉/؉ and Egr-1 ؊/؊ mice exhibited similar survival times in a model of acute endotoxemia. These data indicate that Egr-1 does not contribute to the early inflammatory response in the kidneys and lungs or the early systemic inflammatory response in endotoxemic mice. However, Egr-1 does contribute to the sustained expression of inflammatory mediators and to the maximal expression of TF at 8 hours in the kidneys and lungs. IntroductionSeptic shock is induced in humans by the presence of pathogenic bacteria or fungi in the blood and is associated with a high mortality. 1 In Gram-negative sepsis, lipopolysaccharide (LPS [endotoxin]) is released from Gram-negative bacteria and activates monocytes, endothelial cells, and epithelial cells. In sepsis, the procoagulant molecule tissue factor (TF) is expressed by circulating monocytes, vascular endothelial cells in the spleen, and epithelial cells in the lungs and kidneys. 2-7 TFdependent activation of coagulation and the resulting intravascular fibrin deposition contributes to multiorgan failure. 8 Administration of anti-TF antibodies reduced mortality in baboon and mouse models of septic shock. 9,10 In addition, administration of other coagulation inhibitors, such as antithrombin III, protein C, and tissue factor pathway inhibitor in various animal models of sepsis, reduced mortality. [11][12][13] Plasminogen activator inhibitor type 1 (PAI-1) inhibits both types of plasminogen activators and reduces fibrinolysis. 14 PAI-1 activity is increased in the plasma of patients with Gram-negative sepsis 15 and is likely to contribute to intravascular fibrin deposition. Indeed, inhibition of PAI-1 prevents renal fibrin deposition in endotoxemic rabbits. 16 In a mouse model of endotoxemia, maximal levels of TF mRNA are observed at 8 hours, and induction is observed in bronchial and tubular epithelial cells in the lungs and kidneys, respectively. 2,[5][6][7] In contrast, LPS treatment of mice induces maximal PAI-1 mRNA expression at 3 hours, and PAI-1 is expressed by endot...

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“…Among the changes observed on exposure to LPS are fever, circulatory shock, disseminated intravascular coagulation, and damage to numerous organs, including the liver. 8 Although the mechanisms contributing to tissue injury by LPS are many and may vary among tissues, a commonality appears to be the involvement of host-derived, soluble and cellular mediators of inflammation. 9 Interactions among several of these appear to be necessary for full manifestation of tissue injury during LPS exposure.…”

mentioning

confidence: 99%

Bacterial Lipopolysaccharide Enhances Aflatoxin B1 Hepatotoxicity in Rats by A Mechanism That Depends on Tumor Necrosis Factor α

Barton

Ganey

et al. 2001

Hepatology

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Endotoxin-induced organ injury

Cited by 106 publications

References 0 publications

Increased Cholesterol Deposition, Expression of Scavenger Receptors, and Response to Chemotactic Factors in Abca1 -Deficient Macrophages

Increased Cholesterol Deposition, Expression of Scavenger Receptors, and Response to Chemotactic Factors in Abca1 -Deficient Macrophages

Regulation of tissue factor and inflammatory mediators by Egr-1 in a mouse endotoxemia model

Bacterial Lipopolysaccharide Enhances Aflatoxin B1 Hepatotoxicity in Rats by A Mechanism That Depends on Tumor Necrosis Factor α

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