Preconditioning with high mobility group box 1 (HMGB1) induces lipopolysaccharide (LPS) tolerance

Aneja, Rajesh K.; Tsung, Allan; Sjodin, Hanna; Gefter, Julia V.; Delude, Russell L.; Billiar, Timothy R.; Fink, Mitchell P.

doi:10.1189/jlb.0108030

Cited by 61 publications

(60 citation statements)

References 44 publications

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“…Various receptors are known to interact with HSP70 and HMGB1 and, among them, TLR4 and TLR2 seems to be important in mediating HSP70-and HMGB1-induced inflammatory responses (19,20,(32)(33)(34)(35)(36)(37). These receptors are known to respond to HSP70 and HMGB1 only after binding to other molecules (22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

Macrophage Inflammatory Protein Derivative ECI301 Enhances the Alarmin-Associated Abscopal Benefits of Tumor Radiotherapy

et al. 2014

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Radiotherapy can produce antitumor benefits beyond the local site of irradiation, an immune-based phenomenon known as the abscopal effect, but the mechanisms underlying these benefits are poorly understood. Preclinical studies of ECI301, a mutant derivative of macrophage inhibitory protein-1a, have shown that its administration can improve the antitumor effects of radiotherapy in a manner associated with a tumorindependent abscopal effect. In this article, we report that i.v. administration of ECI301 after intratumoral injection of tumor cell lysates can inhibit tumor growth, not only at the site of injection but also at nontreated sites. Effects of the tumor lysate were further recapitulated by i.v. administration of the alarmins HSP70 or HMGB1, but not HSP60, and combinations of ECI301 þ HSP70 were sufficient to inhibit tumor growth. Although injection of ECI301 þ HMGB1 did not inhibit tumor growth, we found that administration of a neutralizing HMGB1 antibody neutralized the cooperative effects of ECI301 on tumor irradiation. Moreover, mice genetically deficient in TLR4, an immune pattern receptor that binds alarmins, including HMGB1 and HSP70, did not exhibit antitumor responses to irradiation with ECI301 administration. Although ECI301 was cleared rapidly from peripheral blood, it was found to bind avidly to HSP70 and HMGB1 in vitro. Our results suggest a model in which sequential release of the alarmins HSP70 and HMGB1 from a tumor by irradiation may trap circulating ECI301, thereby licensing or restoring tumor immunosurveillance capabilities of natural killer cells or CD4 þ and CD8 þ T cells against tumor cells that may evade irradiation. Cancer Res; 74(18); 5070-8. Ó2014 AACR.

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Section: Discussionmentioning

confidence: 99%

Macrophage Inflammatory Protein Derivative ECI301 Enhances the Alarmin-Associated Abscopal Benefits of Tumor Radiotherapy

et al. 2014

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“…Interestingly, it has been shown that another endogenous TLR4 agonist, HMGB1, could induce LPS tolerance of monocyte lineage cells in a RAGE-dependent manner. 50 Therefore, there is intersection between RAGE and TLR4 BLOOD, 13 SEPTEMBER 2012 ⅐ VOLUME 120, NUMBER 11 For personal use only. on June 19, 2019.…”

Section: Discussionmentioning

confidence: 99%

Myeloid skewing in murine autoimmune arthritis occurs in hematopoietic stem and primitive progenitor cells

Oduro¹,

Liu²,

Tan³

et al. 2012

Blood

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Skewing toward myeloid cell production is often observed in chronic inflammation and autoimmune diseases. Herein, we determined whether persistent myeloid activation and proinflammatory output occurring in pathologic conditions is at the level of hematopoietic stem and primitive progenitor cells (HSPPCs). By using a mouse arthritis model, we found that even though HSPPCs in arthritis still retained the capacity to differentiate into different lineages, they acquired enhanced in vitro and in vivo propensity in a disease-dependent manner to generate myeloid cells, the key perpetrators of tissue damage in arthritis. This myeloid skewing was cell intrinsic, as arthritic HSPPCs up-regulate myeloid-specific transcripts including S100a8. Exogenous S100a8 promoted myeloid cell output from wild-type HSPPCs, suggesting mechanistic involvement of this gene in the myeloid priming that occurs in arthritic HSPPCs. Therefore, our results indicate that in arthritic mice, HSPPCs adopt a pathologic state that favors disease persistence.

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“…Alternately, it may underscore that the plasma level of HMGB1 is critical for the survival of endotoxemia or sepsis. Although it is difficult to explain how CO inhibits the release HMGB1 at the present time, CO can inhibit nuclear factor-B activity or p38 mitogen-activated protein kinase (Ulloa et al, 2002;Bonaldi et al, 2003;Aneja et al, 2008) or activate peroxisome proliferator-activated receptor-␥ (Hoetzel et al, 2008). Therefore, further study is needed to determine whether possible mechanism(s) of CO exerts on the HMGB1 release by LPS-or CLP-induced sepsis.…”

Section: Co Inhibits Hmgb1 Release In Lps-and Clp-induced Sepsis 179mentioning

confidence: 99%

Heme-Oxygenase-1 Induction and Carbon Monoxide-Releasing Molecule Inhibit Lipopolysaccharide (LPS)-Induced High-Mobility Group Box 1 Release in Vitro and Improve Survival of Mice in LPS- and Cecal Ligation and Puncture-Induced Sepsis Model in Vivo

Tsoyi

Lee²,

Lee³

et al. 2009

Mol Pharmacol

180

110

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We examined our hypothesis that heme-oxygenase-1 (HO-1)-derived carbon monoxide (CO) inhibits the release of highmobility group box 1 (HMGB1) in RAW264.7 cells activated with lipopolysaccharide (LPS) in vitro and in LPS-or cecal ligation and puncture (CLP)-induced septic mice in vivo, so that HO-1 induction or CO improves survival of sepsis in rodents. We found that pretreatment with HO-1 inducers (hemin, cobalt protoporphyrin IX) or transfection of HO-1 significantly inhibited HMGB1 release, which was blocked by HO-1 small interfering RNA, in cells activated by LPS. Carbon monoxide-releasing molecule 2 (CORM-2) but not bilirubin or deferoxamine inhibited HMGB1 release in LPS-activated macrophages. Oxyhemoglobin reversed the effect of HO-1 inducers on HMGB1 release. Translocation of HMGB1 from nucleus to cytosol was significantly inhibited by HO-1 inducers, CORM-2, or HO-1 transfection. Neutralizing antibodies to tumor necrosis factor (TNF)-␣, interleukin (IL)-1␤, interferon-␤, and N -nitro-L-arginine methyl ester hydrochloride but not N-[2-(cyclohexyloxyl)-4-nitrophenyl]-methane sulfonamide (NS-398) significantly inhibited HMGB1 release in LPS-activated cells. Production of TNF-␣, IL-1␤, and IFN-␤ was significantly reduced by pretreatment of HO-1 inducers, CORM-2, or HO-1 transfection in LPS-activated cells. Plasma levels of HMGB1 in mice challenged with LPS or CLP were significantly reduced by the administration of HO-1 inducers or CORM-2, which was accompanied by either reduction (pretreatment) or no change (delayed administration) of serum TNF-␣ and IL-1␤ levels. Regardless of pretreatment or delayed administration, CORM-2 and hemin rescued mice from lethal endotoxemia and sepsis induced by LPS or CLP. Taken together, we concluded that HO-1-derived CO reduces HMGB1 release in LPS-activated cells and LPS-or CLP-induced animal model of sepsis.Sepsis is defined as a systemic inflammatory response syndrome from a microbial infection that results from excessive stimulation of the host immune system by pathogen components to produce various proinflammatory cytokines, and their overproduction causes systemic inflammation that can lead to the lethal multiple organ damage (Oberholzer et al., 2001). High-mobility group box 1 (HMGB1) is a chromatin-binding protein that participates in maintaining nucleosome structure and regulation of gene transcription (Landsman and Bustin, 1993). Various evidence indicated that HMGB1 is a necessary and sufficient late mediator of severe sepsis (Wang et al., 1999;Yang et al., 2004). Once released, HMGB1 can bind to cell-surface receptors, such as the receptor for advanced glycation end products and Toll-like receptors 2 and 4, and mediate various cellular responses, chemotactic cell movement, and release of proinflammatory Article, publication date, and citation information can be found at http://molpharm.aspetjournals.org. doi:10.1124/mol.109.055137.ABBREVIATIONS: HMGB1, high-mobility group box 1; HO-1, heme-oxygenase-1; CORM-2, carbon monoxide-releasing molecule II; LPS, lip...

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Preconditioning with high mobility group box 1 (HMGB1) induces lipopolysaccharide (LPS) tolerance

Cited by 61 publications

References 44 publications

Macrophage Inflammatory Protein Derivative ECI301 Enhances the Alarmin-Associated Abscopal Benefits of Tumor Radiotherapy

Macrophage Inflammatory Protein Derivative ECI301 Enhances the Alarmin-Associated Abscopal Benefits of Tumor Radiotherapy

Myeloid skewing in murine autoimmune arthritis occurs in hematopoietic stem and primitive progenitor cells

Heme-Oxygenase-1 Induction and Carbon Monoxide-Releasing Molecule Inhibit Lipopolysaccharide (LPS)-Induced High-Mobility Group Box 1 Release in Vitro and Improve Survival of Mice in LPS- and Cecal Ligation and Puncture-Induced Sepsis Model in Vivo

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