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Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice
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| Veröffentlicht in: | Frontiers in immunology 8(2017) Artikel-Nummer 1672, 13 Seiten |
|---|---|
| Personen und Körperschaften: | , |
| Titel: | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice/ Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
28 November 2017
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| Gesamtaufnahme: |
: Frontiers in immunology, 8(2017) Artikel-Nummer 1672, 13 Seiten
, volume:8 |
| Schlagwörter: | |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 245 | 1 | 0 | |a Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice |c Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar |
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| 520 | |a Trauma combined with hemorrhagic shock (HS/T) leads to systemic inflammation that results in organ injury. Toll-like Receptor 4 (TLR4)-signaling activation contributes to the initiation of inflammatory pathways following HS/T but its cell-specific roles in this setting are not known. We assessed the importance of TLR4 on leukocytes of myeloid lineage and dendritic cells (DC) to the early systemic inflammatory response following HS/T. Mice were subjected to HS/T and 20 inflammatory mediators were measured in plasma followed by Dynamic Bayesian Network (DBN) Analysis. Organ damage was assessed by histology and plasma ALT levels. The role of TLR4 was determined using TLR4-/-, MyD88-/-, and Trif-/- C57BL/6 (B6) mice, and by in vivo administration of a TLR4-specific neutralizing monoclonal antibody (mAb). The contribution of TLR4 expressed by myeloid leukocytes and DC was determined by generating cell-specific TLR4-/- B6 mice, including Lyz-Cre x TLR4loxP/loxP, and CD11c-Cre x TLR4loxP/loxP B6 mice. Adoptive transfer of bone marrow-derived TLR4+/+ or TLR4-/- DC into TLR4-/- mice confirmed the contribution of TLR4 on DC to the systemic inflammatory response after HS/T. Using both global knockout mice and the TLR4 blocking mAb 1A6 we established a central role for TLR4 in driving systemic inflammation. Using cell-selective TLR4-/- B6 mice we found that TLR4 expression on both myeloid cells and CD11chigh DC is required for increases in systemic cytokine levels and organ damage after HS/T. We confirmed the capacity of TLR4 on CD11chigh DC to promote inflammation and liver damage using adoptive transfer of TLR4+/+ conventional (CD11chigh) DC into TLR4-/- mice. DBN inference identified CXC chemokines as proximal drivers of dynamic changes in the circulating levels of cytokines/chemokines after HS/T. TLR4 on DC was found to contribute selectively to the elevations in these proximal drivers. TLR4 on both myeloid cells and conventional DC is required for the initial systemic inflammation and organ damage in a mouse model of HS/T. This includes a role for TLR4 on DC in promoting increases in the early inflammatory networks identified in HS/T. These data establish DC along with macrophages as essential to the recognition of tissue damage and stress following tissue trauma with hemorrhagic shock. | ||
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| contents | Trauma combined with hemorrhagic shock (HS/T) leads to systemic inflammation that results in organ injury. Toll-like Receptor 4 (TLR4)-signaling activation contributes to the initiation of inflammatory pathways following HS/T but its cell-specific roles in this setting are not known. We assessed the importance of TLR4 on leukocytes of myeloid lineage and dendritic cells (DC) to the early systemic inflammatory response following HS/T. Mice were subjected to HS/T and 20 inflammatory mediators were measured in plasma followed by Dynamic Bayesian Network (DBN) Analysis. Organ damage was assessed by histology and plasma ALT levels. The role of TLR4 was determined using TLR4-/-, MyD88-/-, and Trif-/- C57BL/6 (B6) mice, and by in vivo administration of a TLR4-specific neutralizing monoclonal antibody (mAb). The contribution of TLR4 expressed by myeloid leukocytes and DC was determined by generating cell-specific TLR4-/- B6 mice, including Lyz-Cre x TLR4loxP/loxP, and CD11c-Cre x TLR4loxP/loxP B6 mice. Adoptive transfer of bone marrow-derived TLR4+/+ or TLR4-/- DC into TLR4-/- mice confirmed the contribution of TLR4 on DC to the systemic inflammatory response after HS/T. Using both global knockout mice and the TLR4 blocking mAb 1A6 we established a central role for TLR4 in driving systemic inflammation. Using cell-selective TLR4-/- B6 mice we found that TLR4 expression on both myeloid cells and CD11chigh DC is required for increases in systemic cytokine levels and organ damage after HS/T. We confirmed the capacity of TLR4 on CD11chigh DC to promote inflammation and liver damage using adoptive transfer of TLR4+/+ conventional (CD11chigh) DC into TLR4-/- mice. DBN inference identified CXC chemokines as proximal drivers of dynamic changes in the circulating levels of cytokines/chemokines after HS/T. TLR4 on DC was found to contribute selectively to the elevations in these proximal drivers. TLR4 on both myeloid cells and conventional DC is required for the initial systemic inflammation and organ damage in a mouse model of HS/T. This includes a role for TLR4 on DC in promoting increases in the early inflammatory networks identified in HS/T. These data establish DC along with macrophages as essential to the recognition of tissue damage and stress following tissue trauma with hemorrhagic shock. |
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| spelling | Zettel, Kent VerfasserIn (DE-588)1163421448 (DE-627)1027799892 (DE-576)507994450 aut, Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar, 28 November 2017, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Gesehen am 26.07.2018, Trauma combined with hemorrhagic shock (HS/T) leads to systemic inflammation that results in organ injury. Toll-like Receptor 4 (TLR4)-signaling activation contributes to the initiation of inflammatory pathways following HS/T but its cell-specific roles in this setting are not known. We assessed the importance of TLR4 on leukocytes of myeloid lineage and dendritic cells (DC) to the early systemic inflammatory response following HS/T. Mice were subjected to HS/T and 20 inflammatory mediators were measured in plasma followed by Dynamic Bayesian Network (DBN) Analysis. Organ damage was assessed by histology and plasma ALT levels. The role of TLR4 was determined using TLR4-/-, MyD88-/-, and Trif-/- C57BL/6 (B6) mice, and by in vivo administration of a TLR4-specific neutralizing monoclonal antibody (mAb). The contribution of TLR4 expressed by myeloid leukocytes and DC was determined by generating cell-specific TLR4-/- B6 mice, including Lyz-Cre x TLR4loxP/loxP, and CD11c-Cre x TLR4loxP/loxP B6 mice. Adoptive transfer of bone marrow-derived TLR4+/+ or TLR4-/- DC into TLR4-/- mice confirmed the contribution of TLR4 on DC to the systemic inflammatory response after HS/T. Using both global knockout mice and the TLR4 blocking mAb 1A6 we established a central role for TLR4 in driving systemic inflammation. Using cell-selective TLR4-/- B6 mice we found that TLR4 expression on both myeloid cells and CD11chigh DC is required for increases in systemic cytokine levels and organ damage after HS/T. We confirmed the capacity of TLR4 on CD11chigh DC to promote inflammation and liver damage using adoptive transfer of TLR4+/+ conventional (CD11chigh) DC into TLR4-/- mice. DBN inference identified CXC chemokines as proximal drivers of dynamic changes in the circulating levels of cytokines/chemokines after HS/T. TLR4 on DC was found to contribute selectively to the elevations in these proximal drivers. TLR4 on both myeloid cells and conventional DC is required for the initial systemic inflammation and organ damage in a mouse model of HS/T. This includes a role for TLR4 on DC in promoting increases in the early inflammatory networks identified in HS/T. These data establish DC along with macrophages as essential to the recognition of tissue damage and stress following tissue trauma with hemorrhagic shock., Dendritic Cells, hemorrhagic shock, Myeloid Cells, TLR4, Trauma, Korff, Sebastian 1978- VerfasserIn (DE-588)140496076 (DE-627)618903364 (DE-576)318524481 aut, Enthalten in Frontiers in immunology Lausanne : Frontiers Media, 2010 8(2017) Artikel-Nummer 1672, 13 Seiten Online-Ressource (DE-627)657998354 (DE-600)2606827-8 (DE-576)343624834 1664-3224 nnns, volume:8 year:2017, http://dx.doi.org/10.3389/fimmu.2017.01672 Verlag Resolving-System kostenfrei Volltext, https://www.frontiersin.org/articles/10.3389/fimmu.2017.01672/full Verlag kostenfrei Volltext, http://dx.doi.org/10.3389/fimmu.2017.01672 LFER, LFER 2018-08-13T00:00:00Z |
| spellingShingle | Zettel, Kent, Korff, Sebastian, Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice, Trauma combined with hemorrhagic shock (HS/T) leads to systemic inflammation that results in organ injury. Toll-like Receptor 4 (TLR4)-signaling activation contributes to the initiation of inflammatory pathways following HS/T but its cell-specific roles in this setting are not known. We assessed the importance of TLR4 on leukocytes of myeloid lineage and dendritic cells (DC) to the early systemic inflammatory response following HS/T. Mice were subjected to HS/T and 20 inflammatory mediators were measured in plasma followed by Dynamic Bayesian Network (DBN) Analysis. Organ damage was assessed by histology and plasma ALT levels. The role of TLR4 was determined using TLR4-/-, MyD88-/-, and Trif-/- C57BL/6 (B6) mice, and by in vivo administration of a TLR4-specific neutralizing monoclonal antibody (mAb). The contribution of TLR4 expressed by myeloid leukocytes and DC was determined by generating cell-specific TLR4-/- B6 mice, including Lyz-Cre x TLR4loxP/loxP, and CD11c-Cre x TLR4loxP/loxP B6 mice. Adoptive transfer of bone marrow-derived TLR4+/+ or TLR4-/- DC into TLR4-/- mice confirmed the contribution of TLR4 on DC to the systemic inflammatory response after HS/T. Using both global knockout mice and the TLR4 blocking mAb 1A6 we established a central role for TLR4 in driving systemic inflammation. Using cell-selective TLR4-/- B6 mice we found that TLR4 expression on both myeloid cells and CD11chigh DC is required for increases in systemic cytokine levels and organ damage after HS/T. We confirmed the capacity of TLR4 on CD11chigh DC to promote inflammation and liver damage using adoptive transfer of TLR4+/+ conventional (CD11chigh) DC into TLR4-/- mice. DBN inference identified CXC chemokines as proximal drivers of dynamic changes in the circulating levels of cytokines/chemokines after HS/T. TLR4 on DC was found to contribute selectively to the elevations in these proximal drivers. TLR4 on both myeloid cells and conventional DC is required for the initial systemic inflammation and organ damage in a mouse model of HS/T. This includes a role for TLR4 on DC in promoting increases in the early inflammatory networks identified in HS/T. These data establish DC along with macrophages as essential to the recognition of tissue damage and stress following tissue trauma with hemorrhagic shock., Dendritic Cells, hemorrhagic shock, Myeloid Cells, TLR4, Trauma |
| swb_id_str | 507994272 |
| title | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice |
| title_auth | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice |
| title_full | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar |
| title_fullStr | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar |
| title_full_unstemmed | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar |
| title_in_hierarchy | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice / Kent Zettel, Sebastian Korff, Ruben Zamora, Adrian E. Morelli, Sophie Darwiche, Patricia A. Loughran, Greg Elson, Limin Shang, Susana Salgado-Pires, Melanie J. Scott, Yoram Vodovotz, Timothy R. Billiar, |
| title_short | Toll-like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice |
| title_sort | toll like receptor 4 on both myeloid cells and dendritic cells is required for systemic inflammation and organ damage after hemorrhagic shock with tissue trauma in mice |
| topic | Dendritic Cells, hemorrhagic shock, Myeloid Cells, TLR4, Trauma |
| topic_facet | Dendritic Cells, hemorrhagic shock, Myeloid Cells, TLR4, Trauma |
| url | http://dx.doi.org/10.3389/fimmu.2017.01672, https://www.frontiersin.org/articles/10.3389/fimmu.2017.01672/full |