HMGB-1 as a Useful Prognostic Biomarker in Sepsis-Induced Organ Failure in Patients Undergoing PMX-DHP

Ueno, Takamasa; Ikeda, Toshiaki; Ikeda, Keisuke; Taniuchi, Hitoshi; Suda, S; Yeung, Melissa Y.; Matsuno, Naoto

doi:10.1016/j.jss.2009.11.708

Cited by 28 publications

(24 citation statements)

References 42 publications

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“…Furthermore, the administration of PPAR γ ligand decreased the endotoxin-induced lethality of LPS in mice and reduced levels of circulating HMGB1, indicating that the effects of PPAR γ on septic shock are HMGB1 dependent. This finding is in line with previous studies in which high levels of HMGB1 were demonstrated in patients with severe sepsis and in animals models of endotoxemia [3, 4, 26, 27], suggesting that HMGB1 may play a crucial role in the process of sepsis. PPAR γ has also been reported to mediate inflammatory responses by inhibiting proinflammatory cytokines, such as TNF- α , interleukin (IL)-6, and iNOS [19, 20, 28].…”

Section: Discussionsupporting

confidence: 92%

Activation of Peroxisome Proliferator-Activated Receptorγby Rosiglitazone Inhibits Lipopolysaccharide-Induced Release of High Mobility Group Box 1

Hwang

Kang

Ham

et al. 2012

Mediators of Inflammation

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Peroxisome proliferator-activated receptors (PPARs) are shown to modulate the pathological status of sepsis by regulating the release of high mobility group box 1 (HMGB1), a well-known late proinflammatory mediator of sepsis. Ligand-activated PPARs markedly inhibited lipopolysaccharide- (LPS) induced release of HMGB1 in RAW 264.7 cells. Among the ligands of PPAR, the effect of rosiglitazone, a specific ligand for PPARγ, was superior in the inhibition of HMGB1 release induced by LPS. This effect was observed in cells that received rosiglitazone before LPS or after LPS treatment, indicating that rosiglitazone is effective in both treatment and prevention. Ablation of PPARγ with small interfering RNA or GW9662-mediated inhibition of PPARγ abolished the effect of rosiglitazone on HMGB1 release. Furthermore, the overexpression of PPARγ markedly potentiated the inhibitory effect of rosiglitazone on HMGB1 release. In addition, rosiglitazone inhibited LPS-induced expression of Toll-like receptor 4 signal molecules, suggesting a possible mechanism by which rosiglitazone modulates HMGB1 release. Notably, the administration of rosiglitazone to mice improved survival rates in an LPS-induced animal model of endotoxemia, where reduced levels of circulating HMGB1 were demonstrated. Taken together, these results suggest that PPARs play an important role in the cellular response to inflammation by inhibiting HMGB1 release.

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Section: Discussionsupporting

confidence: 92%

Activation of Peroxisome Proliferator-Activated Receptorγby Rosiglitazone Inhibits Lipopolysaccharide-Induced Release of High Mobility Group Box 1

Hwang

Kang

Ham

et al. 2012

Mediators of Inflammation

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“…In addition, HMGB-1 is considered to have prognostic significance [91] and is a possible therapeutic target in sepsis syndromes and other inflammatory disorders [92]. In septic rats, high-dose IgG pre-treatment reduced HMGB-1 activity [93].…”

Section: The Biological Rationale For Administering Ivig In Sepsismentioning

confidence: 99%

Bench-to-bedside review: Immunoglobulin therapy for sepsis - biological plausibility from a critical care perspective

et al. 2011

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Sepsis represents a dysregulated host response to infection, the extent of which determines the severity of organ dysfunction and subsequent outcome. All trialled immunomodulatory strategies to date have resulted in either outright failure or inconsistent degrees of success. Intravenous immunoglobulin (IVIg) therapy falls into the latter category with opinion still divided as to its utility. This article provides a narrative review of the biological rationale for using IVIg in sepsis. A literature search was conducted using the PubMed database (1966 to February 2011). The strategy included the following text terms and combinations of these: IVIg, intravenous immune globulin, intravenous immunoglobulin, immunoglobulin, immunoglobulin therapy, pentaglobin, sepsis, inflammation, immune modulation, apoptosis. Preclinical and extrapolated clinical data of IVIg therapy in sepsis suggests improved bacterial clearance, inhibitory effects upon upstream mediators of the host response (for example, the nuclear factor kappa B (NF-κB) transcription factor), scavenging of downstream inflammatory mediators (for example, cytokines), direct anti-inflammatory effects mediated via Fcγ receptors, and a potential ability to attenuate lymphocyte apoptosis and thus sepsis-related immunosuppression. Characterizing the trajectory of change in immunoglobulin levels during sepsis, understanding mechanisms contributing to these changes, and undertaking IVIg dose-finding studies should be performed prior to further large-scale interventional trials to enhance the likelihood of a successful outcome.

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“…Several studies report a reduction in cytokines and inflammatory molecules in patients' plasma after PMX hemoperfusion [54, 56, 61, 68–70]. …”

Section: Immunological Mechanisms Described For Polymyxin B-immobimentioning

confidence: 99%

“…A recent study exploring the meaning of HMGB-1 levels in 60 patients with septic shock treated with PMX hemoperfusion found a significant positive correlation between the Sequential Organ Failure Assessment (SOFA) score and HMGB-1 level ( P < 0.05). The authors concluded that HMGB-1 is a useful prognostic biomarker in sepsis-induced organ failure in patients undergoing PMX hemoperfusion, but formal establishment of the utility of HMGB-1 as a prognostic biomarker still remains to be performed [68]. …”

Section: Immunological Mechanisms Described For Polymyxin B-immobimentioning

confidence: 99%

Immunomodulation in Sepsis: The Role of Endotoxin Removal by Polymyxin B-Immobilized Cartridge

Esteban

Ferrer

Alsina

et al. 2013

Mediators of Inflammation

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Severe sepsis results in high morbidity and mortality. Immunomodulation strategies could be an adjunctive therapy to treat sepsis. Endotoxin is a component of gram-negative bacteria and plays an important role in the pathogenesis of septic shock when it is recognized by immune cells. Removal of endotoxin could be an effective adjunctive approach to the management of sepsis. Devices to adsorb endotoxin or inflammatory cytokines have been designed as a strategy to treat severe sepsis, especially sepsis caused by gram-negative bacteria. Polymyxin B-immobilized cartridge has been successfully used to treat patients with sepsis of abdominal origin. Although this cartridge was conceived to adsorb endotoxin, several other immunological mechanisms have been elucidated, and this device has also yielded promising results in patients with nonseptic respiratory failure. In this paper, we summarize the immune modulation actions of Polymyxin B-immobilized cartridge to explore its potential usefulness beyond endotoxin elimination.

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HMGB-1 as a Useful Prognostic Biomarker in Sepsis-Induced Organ Failure in Patients Undergoing PMX-DHP

Cited by 28 publications

References 42 publications

Activation of Peroxisome Proliferator-Activated Receptorγby Rosiglitazone Inhibits Lipopolysaccharide-Induced Release of High Mobility Group Box 1

Activation of Peroxisome Proliferator-Activated Receptorγby Rosiglitazone Inhibits Lipopolysaccharide-Induced Release of High Mobility Group Box 1

Bench-to-bedside review: Immunoglobulin therapy for sepsis - biological plausibility from a critical care perspective

Immunomodulation in Sepsis: The Role of Endotoxin Removal by Polymyxin B-Immobilized Cartridge

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