High‐mobility group box‐1 in sterile inflammation

Tsung, Allan; Tohme, Samer; Billiar, Timothy R.

doi:10.1111/joim.12276

Cited by 172 publications

(175 citation statements)

References 194 publications

(277 reference statements)

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“…We show here that HMGB1 is released by neutrophils during degranulation and that HMGB1 is postulated to assist in the recognition of extracellular DNA by intracellular TLR9 to activate the protumorigenic pathways (30,31). In addition, we, among others, have shown that HMGB1 is implicated in nearly every step of tumor progression (24,41,42). In addition to HMGB1, other peptides released during NETosis may play a role in tumor progression.…”

Section: Discussionmentioning

confidence: 95%

Neutrophil extracellular traps promote the development and progression of liver metastases after surgical stress

Tohme

Yazdani

Simmons

et al. 2017

HPB

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Risks of tumor recurrence after surgical resection have been known for decades, but the mechanisms underlying treatment failures remain poorly understood. Neutrophils, first-line responders after surgical stress, may play an important role in linking inflammation to cancer progression. In response to stress, neutrophils can expel their protein-studded chromatin to form local snares known as neutrophil extracellular traps (NET). In this study, we asked whether as a result of its ability to ensnare moving cells NET formation might promote metastasis after surgical stress. Consistent with this hypothesis, in a cohort of patients undergoing attempted curative liver resection for metastatic colorectal cancer, we observed that increased postoperative NET formation was associated with a >4-fold reduction in disease-free survival. In like manner, in a murine model of surgical stress employing liver ischemia-reperfusion, we observed an increase in NET formation that correlated with an accelerated development and progression of metastatic disease. These effects were abrogated by inhibiting NET formation in mice, through either local treatment with DNAse or inhibition of the enzyme peptidylarginine deaminase (PAD4), which is essential for NET formation. In growing metastatic tumors, we found that intratumoral hypoxia accentuated NET formation. Mechanistic investigations in vitro indicated that mouse neutrophilderived NET triggered HMGB1 release and activated TLR9-dependent pathways in cancer cells to promote their adhesion, proliferation, migration and invasion. Taken together, our findings implicate NET in the development of liver metastases after surgical stress, suggesting that their elimination may reduce risks of tumor relapse. HHS Public Access

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Section: Discussionmentioning

confidence: 95%

Neutrophil extracellular traps promote the development and progression of liver metastases after surgical stress

Tohme

Yazdani

Simmons

et al. 2017

HPB

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“…hypoxia, senescence and autoimmune disease). The latter happens immediately (Scaffidi et al 2002), whereas the former is a slower mechanism mediated by cellular signal transduction (Tsung et al 2014). Once HMGB1 accumulates in the extracellular milieu, it conveys danger signals by triggering inflammatory pathways, including NF-κB, ERK and p38, in neighboring cells via numerous cell surface receptors such as TLRs 2, 4 and 9; RAGE; CD24; and others (Venereau et al 2013).…”

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

215

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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“…However, being released to extracellular milieu, HMGB1 could bind with its special receptor, TLR4, and exert as a central factor and prompt inflammatory responses during various pathophysiological processes. 17,18) Considering that HMGB1 plays important roles during development of inflammatory responses, researchers have tested whether HMGB1 neutralizing antibody could have beneficial effects on hemorrhagic shock. In their study, they showed that Neutralizing HMGB1 method was also demonstrated to ameliorate gut barrier dysfunction, elevate survival, and attenuate hemorrhagic shock significantly.…”

Section: Treatment Of Anti-hmgb1 Antibody Decreased Lps Induced Inflamentioning

confidence: 99%

HMGB1 Neutralizing Antibody Attenuates Cardiac Injury and Apoptosis Induced by Hemorrhagic Shock/Resuscitation in Rats

Zhou

2015

Biological & Pharmaceutical Bulletin

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High-mobility group box 1 (HMGB1) and its natural receptor, Toll-like receptor-4 (TLR4), are involved in various infectious or noninfectious diseases including hemorrhagic shock. HMGB1 neutralizing antibody (anti-HMGB1 monoclonal antibody (mAb)) treatment was shown to alleviate ischemia-reperfusion injury effectively. The aim of this study was to explore whether and by what mechanisms anti-HMGB1 mAb attenuates hemorrhagic shock and resuscitation (HS/R)-induced cardiac injury. Employing rat HS/R models, we found that anti-HMGB1 mAb treatment improved HS/R-induced cardiac function deterioration, attenuated cardiac enzyme elevation, improved ATP loss, and protected cardiac tissue. Anti-HMGB1 mAb also inhibited the production of inflammatory factors interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). Moreover, anti-HMGB1 mAb reduced apoptotic responses by suppressing activated caspase-3 and reversing apoptotic gene expression of capase-3, Bax, and Bcl-2 in rat cardiac tissue. Moreover, anti-HMGB1 mAb decreased HS/R-induced HMGB1 and TLR4 expression elevation. We further confirmed that anti-HMGB1 mAb inhibited lipopolysaccharide-activated HGMB1 and TLR4 expression and decreased inflammatory factors IL-1β, IL-6, and TNF-α at the cellular level. It was concluded that anti-HMGB1 mAb treatment protects rats from cardiac injury induced by HS/R, and the beneficial effects may be related to its inhibitory effects on the HMGB1-TLR4 axis.

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High‐mobility group box‐1 in sterile inflammation

Abstract: Abstract. Tsung A, Tohme S, Billiar TR

Cited by 172 publications

References 194 publications

Neutrophil extracellular traps promote the development and progression of liver metastases after surgical stress

Neutrophil extracellular traps promote the development and progression of liver metastases after surgical stress

Sterile inflammation and pregnancy complications: a review

HMGB1 Neutralizing Antibody Attenuates Cardiac Injury and Apoptosis Induced by Hemorrhagic Shock/Resuscitation in Rats

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