Early Elevated HMGB1 Level Predicting the Outcome in Exertional Heatstroke

Tong, Huasheng; Tang, Yanhong; Chen, Yi; Qiu, Jun-Ming; Wen, Qiang; Su, Lei

doi:10.1097/ta.0b013e318220b957

Cited by 31 publications

(27 citation statements)

References 33 publications

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“…Peak plasma HMGB1 levels were detected in exertional heat stroke patients within 6 to 13 h of clinical presentation and showed a positive correlation (r = 0.798) with the Acute Physiology and Chronic Health Evaluation II (APACHE II) score (373). The APACHE II score is not specific to heat stroke, but is a clinical classification system used to determine disease severity of ICU patients (187).…”

Section: Biomarkers and Mediators Of Organ Damagementioning

confidence: 99%

“…The APACHE II score is not specific to heat stroke, but is a clinical classification system used to determine disease severity of ICU patients (187). Receiver operating characteristic curve (ROC) analysis identified HMGB1 as having similar sensitivity and specificity as the APACHE II score for prediction of heat stroke lethality (373). In a rat classic heat stroke model, plasma and liver HMGB1 levels were significantly increased at 77 min of heat exposure (body temperature = 43…”

Section: Biomarkers and Mediators Of Organ Damagementioning

confidence: 99%

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Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

319

356

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Heat stroke is a life-threatening condition clinically diagnosed as a severe elevation in body temperature with central nervous system dysfunction that often includes combativeness, delirium, seizures, and coma. Classic heat stroke primarily occurs in immunocompromised individuals during annual heat waves. Exertional heat stroke is observed in young fit individuals performing strenuous physical activity in hot or temperature environments. Long-term consequences of heat stroke are thought to be due to a systemic inflammatory response syndrome. This article provides a comprehensive review of recent advances in the identification of risk factors that predispose to heat stroke, the role of endotoxin and cytokines in mediation of multi-organ damage, the incidence of hypothermia and fever during heat stroke recovery, clinical biomarkers of organ damage severity, and protective cooling strategies. Risk factors include environmental factors, medications, drug use, compromised health status, and genetic conditions. The role of endotoxin and cytokines is discussed in the framework of research conducted over 30 years ago that requires reassessment to more clearly identify the role of these factors in the systemic inflammatory response syndrome. We challenge the notion that hypothalamic damage is responsible for thermoregulatory disturbances during heat stroke recovery and highlight recent advances in our understanding of the regulated nature of these responses. The need for more sensitive clinical biomarkers of organ damage is examined. Conventional and emerging cooling methods are discussed with reference to protection against peripheral organ damage and selective brain cooling.

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Section: Biomarkers and Mediators Of Organ Damagementioning

confidence: 99%

Section: Biomarkers and Mediators Of Organ Damagementioning

confidence: 99%

Heat Stroke

Leon

Bouchama

2015

Comprehensive Physiology

319

356

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“…bacteria and viruses) or other stressors (e.g. oxidative stress and cytokines), which have been shown in immune cells and non-immune cells (Tsung et al 2007, Tang et al 2011, Harris et al 2012. Secondly, whereas (ii) passive release is observed following tissue injury and cell death, especially necrosis (Scaffidi et al 2002) and in specific cases of apoptosis (Qin et al 2006) -including when triggered by sterile injury events (e.g.…”

Section: Hmgb1mentioning

confidence: 99%

“…Of interest, HMGB1 has also been shown to form complexes with many pro-inflammatory mediators and enhance their respective actions in a synergistic manner (Hreggvidsdottir et al 2009). Furthermore, HMGB1 levels are elevated in multiple animal models of sterile injurious events (Tsung et al 2014) and in humans with acute organ injury, autoimmune diseases or cancer (Tong et al 2011. In vitro and in vivo, HMGB1 administration induces inflammation (Yang et al 2005), and more importantly, HMGB1 antagonism protects against sepsis (Yang et al 2004).…”

Section: Hmgb1mentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

204

161

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Inflammation is essential for successful embryo implantation, pregnancy maintenance and delivery. In the last decade, important advances have been made in regard to endogenous, and therefore non-infectious, initiators of inflammation, which can act through the same receptors as pathogens. These molecules are referred to as damage-associated molecular patterns (DAMPs), and their involvement in reproduction has only recently been unraveled. Even though inflammation is necessary for successful reproduction, untimely activation of inflammatory processes can have devastating effect on pregnancy outcomes. Many DAMPs, such as uric acid, high-mobility group box 1 (HMGB1), interleukin (IL)-1 and cell-free fetal DNA, have been associated with pregnancy complications, such as miscarriages, preeclampsia and preterm birth in preclinical models and in humans. However, the specific contribution of alarmins to these conditions is still under debate, as currently there is lack of information on their mechanism of action. In this review, we discuss the role of sterile inflammation in reproduction, including early implantation and pregnancy complications. Particularly, we focus on major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA (especially that of fetal origin) while giving an overview of the potential role of other candidate alarmins.Reproduction (2016) 152 R277-R292

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“…HMGB1 also acts extracellularly as a cytokine, in processes such as inflammation, cell migration and stem cell recruitment. Plasma HMGB1 level at admission is an indicator of the severity of illness and a useful mortality predictor in exertional heatstroke [20]. HMGB1 circulatory levels have been predictors of outcome in neuroinflammation, ischemia reperfusion injury and sepsis [11], [21], [22], [23], [24], [25].…”

Section: Introductionmentioning

confidence: 99%

HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease

et al. 2017

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Recent clinical studies found a strong association of colonic inflammation and Inflammatory bowel disease (IBD)-like phenotype with NonAlcoholic Fatty liver Disease (NAFLD) yet the mechanisms remain unknown. The present study identifies high mobility group box 1 (HMGB1) as a key mediator of intestinal inflammation in NAFLD and outlines a detailed redox signaling mechanism for such a pathway. NAFLD mice showed liver damage and release of elevated HMGB1 in systemic circulation and increased intestinal tyrosine nitration that was dependent on NADPH oxidase. Intestines from NAFLD mice showed higher Toll like receptor 4 (TLR4) activation and proinflammatory cytokine release, an outcome strongly dependent on the existence of NAFLD pathology and NADPH oxidase. Mechanistically intestinal epithelial cells showed the HMGB1 activation of TLR-4 was both NADPH oxidase and peroxynitrite dependent with the latter being formed by the activation of NADPH oxidase. Proinflammatory cytokine production was significantly blocked by the specific peroxynitrite scavenger phenyl boronic acid (FBA), AKT inhibition and NADPH oxidase inhibitor Apocynin suggesting NADPH oxidase-dependent peroxynitrite is a key mediator in TLR-4 activation and cytokine release via an AKT dependent pathway. Studies to ascertain the mechanism of HMGB1-mediated NADPH oxidase activation showed a distinct role of Receptor for advanced glycation end products (RAGE) as the use of inhibitors targeted against RAGE or use of deformed HMGB1 protein prevented NADPH oxidase activation, peroxynitrite formation, TLR4 activation and finally cytokine release. Thus, in conclusion the present study identifies a novel role of HMGB1 mediated inflammatory pathway that is RAGE and redox signaling dependent and helps promote ectopic intestinal inflammation in NAFLD.

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Early Elevated HMGB1 Level Predicting the Outcome in Exertional Heatstroke

Abstract: HMGB1 level at admission is an indicator of the severity of illness and a useful mortality predictor in exertional heatstroke.

Cited by 31 publications

References 33 publications

Heat Stroke

Heat Stroke

Sterile inflammation and pregnancy complications: a review

HMGB1-RAGE pathway drives peroxynitrite signaling-induced IBD-like inflammation in murine nonalcoholic fatty liver disease

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