Role of toll-like receptors 2 and 4, and the receptor for advanced glycation end products in high-mobility group box 1-induced inflammation in vivo

High-mobility group box 1 (HMGB-1) has been reported as a "late" proinflammatory mediator in sepsis. In vitro data have shown that HMGB-1 can induce activation of intracellular signaling pathways via interaction with at least three pattern recognition receptors: Toll-like receptor (TLR) 2,...

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Veröffentlicht in:	Shock (Augusta, Ga.) Jg. 31; H. 3; S. 280
Hauptverfasser:	van Zoelen, Marieke A D, Yang, Huan, Florquin, Sandrine, Meijers, Joost C M, Akira, Shizuo, Arnold, Bernd, Nawroth, Peter P, Bierhaus, Angelika, Tracey, Kevin J, van der Poll, Tom
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States 01.03.2009
Schlagworte:	Animals Antithrombin III - genetics Antithrombin III - metabolism Cytokines - genetics Cytokines - metabolism Female HMGB1 Protein - toxicity Inflammation - chemically induced Inflammation - genetics Inflammation - metabolism Inflammation - mortality Inflammation Mediators - toxicity Male Mice Mice, Knockout Neutrophils - metabolism Neutrophils - pathology Peptide Hydrolases - genetics Peptide Hydrolases - metabolism Receptor for Advanced Glycation End Products Receptors, Immunologic - genetics Receptors, Immunologic - metabolism Time Factors Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism
ISSN:	1540-0514, 1540-0514
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Abstract	High-mobility group box 1 (HMGB-1) has been reported as a "late" proinflammatory mediator in sepsis. In vitro data have shown that HMGB-1 can induce activation of intracellular signaling pathways via interaction with at least three pattern recognition receptors: Toll-like receptor (TLR) 2, TLR-4, and the receptor for advanced glycation end products (RAGE). The objective of this study was to investigate the role of these receptors in the in vivo response to HMGB-1. Therefore, we first performed a time-series experiment with wild-type (Wt) mice. High-mobility group box 1 induced time-dependent elevations of TNF-alpha, IL-6, monocyte chemoattractant protein 1, and thrombin-antithrombin complex levels in peritoneal lavage fluid and plasma. This inflammatory reaction was accompanied by a prominent and sustained rise in neutrophil counts in the peritoneal cavity. We next administered HMGB-1 to Wt, TLR-2, TLR-4, and RAGE mice. All genotypes showed similar plasma levels of TNF-alpha, IL-6, IL-10, and thrombin-antithrombin complex at 2 h after intraperitoneal injection of HMGB-1. Compared with Wt mice, both TLR-4 and RAGE mice displayed lower TNF-alpha and IL-6 concentrations and lower neutrophil numbers in their peritoneal lavage fluid. In contrast, TLR-2 mice showed increased levels of TNF-alpha and IL-6 in their peritoneal cavity relative to Wt mice. These data indicate that HMGB-1 induces release of cytokines, activation of coagulation, and neutrophil recruitment in vivo via a mechanism that at least in part depends on TLR-4 and RAGE.
AbstractList	High-mobility group box 1 (HMGB-1) has been reported as a "late" proinflammatory mediator in sepsis. In vitro data have shown that HMGB-1 can induce activation of intracellular signaling pathways via interaction with at least three pattern recognition receptors: Toll-like receptor (TLR) 2, TLR-4, and the receptor for advanced glycation end products (RAGE). The objective of this study was to investigate the role of these receptors in the in vivo response to HMGB-1. Therefore, we first performed a time-series experiment with wild-type (Wt) mice. High-mobility group box 1 induced time-dependent elevations of TNF-alpha, IL-6, monocyte chemoattractant protein 1, and thrombin-antithrombin complex levels in peritoneal lavage fluid and plasma. This inflammatory reaction was accompanied by a prominent and sustained rise in neutrophil counts in the peritoneal cavity. We next administered HMGB-1 to Wt, TLR-2, TLR-4, and RAGE mice. All genotypes showed similar plasma levels of TNF-alpha, IL-6, IL-10, and thrombin-antithrombin complex at 2 h after intraperitoneal injection of HMGB-1. Compared with Wt mice, both TLR-4 and RAGE mice displayed lower TNF-alpha and IL-6 concentrations and lower neutrophil numbers in their peritoneal lavage fluid. In contrast, TLR-2 mice showed increased levels of TNF-alpha and IL-6 in their peritoneal cavity relative to Wt mice. These data indicate that HMGB-1 induces release of cytokines, activation of coagulation, and neutrophil recruitment in vivo via a mechanism that at least in part depends on TLR-4 and RAGE.High-mobility group box 1 (HMGB-1) has been reported as a "late" proinflammatory mediator in sepsis. In vitro data have shown that HMGB-1 can induce activation of intracellular signaling pathways via interaction with at least three pattern recognition receptors: Toll-like receptor (TLR) 2, TLR-4, and the receptor for advanced glycation end products (RAGE). The objective of this study was to investigate the role of these receptors in the in vivo response to HMGB-1. Therefore, we first performed a time-series experiment with wild-type (Wt) mice. High-mobility group box 1 induced time-dependent elevations of TNF-alpha, IL-6, monocyte chemoattractant protein 1, and thrombin-antithrombin complex levels in peritoneal lavage fluid and plasma. This inflammatory reaction was accompanied by a prominent and sustained rise in neutrophil counts in the peritoneal cavity. We next administered HMGB-1 to Wt, TLR-2, TLR-4, and RAGE mice. All genotypes showed similar plasma levels of TNF-alpha, IL-6, IL-10, and thrombin-antithrombin complex at 2 h after intraperitoneal injection of HMGB-1. Compared with Wt mice, both TLR-4 and RAGE mice displayed lower TNF-alpha and IL-6 concentrations and lower neutrophil numbers in their peritoneal lavage fluid. In contrast, TLR-2 mice showed increased levels of TNF-alpha and IL-6 in their peritoneal cavity relative to Wt mice. These data indicate that HMGB-1 induces release of cytokines, activation of coagulation, and neutrophil recruitment in vivo via a mechanism that at least in part depends on TLR-4 and RAGE. High-mobility group box 1 (HMGB-1) has been reported as a "late" proinflammatory mediator in sepsis. In vitro data have shown that HMGB-1 can induce activation of intracellular signaling pathways via interaction with at least three pattern recognition receptors: Toll-like receptor (TLR) 2, TLR-4, and the receptor for advanced glycation end products (RAGE). The objective of this study was to investigate the role of these receptors in the in vivo response to HMGB-1. Therefore, we first performed a time-series experiment with wild-type (Wt) mice. High-mobility group box 1 induced time-dependent elevations of TNF-alpha, IL-6, monocyte chemoattractant protein 1, and thrombin-antithrombin complex levels in peritoneal lavage fluid and plasma. This inflammatory reaction was accompanied by a prominent and sustained rise in neutrophil counts in the peritoneal cavity. We next administered HMGB-1 to Wt, TLR-2, TLR-4, and RAGE mice. All genotypes showed similar plasma levels of TNF-alpha, IL-6, IL-10, and thrombin-antithrombin complex at 2 h after intraperitoneal injection of HMGB-1. Compared with Wt mice, both TLR-4 and RAGE mice displayed lower TNF-alpha and IL-6 concentrations and lower neutrophil numbers in their peritoneal lavage fluid. In contrast, TLR-2 mice showed increased levels of TNF-alpha and IL-6 in their peritoneal cavity relative to Wt mice. These data indicate that HMGB-1 induces release of cytokines, activation of coagulation, and neutrophil recruitment in vivo via a mechanism that at least in part depends on TLR-4 and RAGE.
Author	Tracey, Kevin J van Zoelen, Marieke A D Arnold, Bernd Nawroth, Peter P van der Poll, Tom Florquin, Sandrine Yang, Huan Meijers, Joost C M Akira, Shizuo Bierhaus, Angelika
Author_xml	– sequence: 1 givenname: Marieke A D surname: van Zoelen fullname: van Zoelen, Marieke A D email: M.A.vanZoelen@amc.uva.nl organization: Center for Infection and Immunity Amsterdam and daggerCenter for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. M.A.vanZoelen@amc.uva.nl – sequence: 2 givenname: Huan surname: Yang fullname: Yang, Huan – sequence: 3 givenname: Sandrine surname: Florquin fullname: Florquin, Sandrine – sequence: 4 givenname: Joost C M surname: Meijers fullname: Meijers, Joost C M – sequence: 5 givenname: Shizuo surname: Akira fullname: Akira, Shizuo – sequence: 6 givenname: Bernd surname: Arnold fullname: Arnold, Bernd – sequence: 7 givenname: Peter P surname: Nawroth fullname: Nawroth, Peter P – sequence: 8 givenname: Angelika surname: Bierhaus fullname: Bierhaus, Angelika – sequence: 9 givenname: Kevin J surname: Tracey fullname: Tracey, Kevin J – sequence: 10 givenname: Tom surname: van der Poll fullname: van der Poll, Tom
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/19218854$$D View this record in MEDLINE/PubMed
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Snippet	High-mobility group box 1 (HMGB-1) has been reported as a "late" proinflammatory mediator in sepsis. In vitro data have shown that HMGB-1 can induce activation...
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SubjectTerms	Animals Antithrombin III - genetics Antithrombin III - metabolism Cytokines - genetics Cytokines - metabolism Female HMGB1 Protein - toxicity Inflammation - chemically induced Inflammation - genetics Inflammation - metabolism Inflammation - mortality Inflammation Mediators - toxicity Male Mice Mice, Knockout Neutrophils - metabolism Neutrophils - pathology Peptide Hydrolases - genetics Peptide Hydrolases - metabolism Receptor for Advanced Glycation End Products Receptors, Immunologic - genetics Receptors, Immunologic - metabolism Time Factors Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - metabolism Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism
Title	Role of toll-like receptors 2 and 4, and the receptor for advanced glycation end products in high-mobility group box 1-induced inflammation in vivo
URI	https://www.ncbi.nlm.nih.gov/pubmed/19218854 https://www.proquest.com/docview/66928264
Volume	31
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