TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance
Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm th...
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| Published in: | PLoS pathogens Vol. 10; no. 1; p. e1003900 |
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| Main Authors: | , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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01-01-2014
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| Abstract | Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1. Trem1(-/-) mice are viable, fertile and show no altered hematopoietic compartment. In CD4(+) T cell- and dextran sodium sulfate-induced models of colitis, Trem1(-/-) mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. Trem1(-/-) mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major. Furthermore, reduced morbidity was observed for influenza virus-infected Trem1(-/-) mice. Importantly, while immune-associated pathologies were significantly reduced, Trem1(-/-) mice were equally capable of controlling infections with L. major, influenza virus, but also Legionella pneumophila as Trem1(+/+) controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control. |
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| AbstractList | Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1. Trem1(-/-) mice are viable, fertile and show no altered hematopoietic compartment. In CD4(+) T cell- and dextran sodium sulfate-induced models of colitis, Trem1(-/-) mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. Trem1(-/-) mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major. Furthermore, reduced morbidity was observed for influenza virus-infected Trem1(-/-) mice. Importantly, while immune-associated pathologies were significantly reduced, Trem1(-/-) mice were equally capable of controlling infections with L. major, influenza virus, but also Legionella pneumophila as Trem1(+/+) controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control. Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1. [Trem1.sup.-/-] mice are viable, fertile and show no altered hematopoietic compartment. In [CD4.sup.+] T cell- and dextran sodium sulfate- induced models of colitis, [Trem1.sup.-/-] mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. [Trem1.sup.-/-] mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major. Furthermore, reduced morbidity was observed for influenza virus-infected [Trem1.sup.-/-] mice. Importantly, while immune-associated pathologies were significantly reduced, [Trem1.sup.-/-] mice were equally capable of controlling infections with L. major, influenza virus, but also Legionella pneumophila as [Trem.sup.1+/+] controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control. Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1. Trem1-/- mice are viable, fertile and show no altered hematopoietic compartment. In CD4+ T cell- and dextran sodium sulfate-induced models of colitis, Trem1-/- mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. Trem1-/- mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major. Furthermore, reduced morbidity was observed for influenza virus-infected Trem1-/- mice. Importantly, while immune-associated pathologies were significantly reduced, Trem1-/- mice were equally capable of controlling infections with L. major, influenza virus, but also Legionella pneumophila as Trem1+/+ controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control. Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses likely aid an improved detection and elimination of pathogens, excessive production of cytokines and oxygen radicals can also severely harm the host. Studies addressing the pathogenic role of TREM-1 during endotoxin-induced shock or microbial sepsis have so far mostly relied on the administration of TREM-1 fusion proteins or peptides representing part of the extracellular domain of TREM-1. However, binding of these agents to the yet unidentified TREM-1 ligand could also impact signaling through alternative receptors. More importantly, controversial results have been obtained regarding the requirement of TREM-1 for microbial control. To unambiguously investigate the role of TREM-1 in homeostasis and disease, we have generated mice deficient in Trem1 . Trem1 −/− mice are viable, fertile and show no altered hematopoietic compartment. In CD4 + T cell- and dextran sodium sulfate-induced models of colitis, Trem1 −/− mice displayed significantly attenuated disease that was associated with reduced inflammatory infiltrates and diminished expression of pro-inflammatory cytokines. Trem1 −/− mice also exhibited reduced neutrophilic infiltration and decreased lesion size upon infection with Leishmania major . Furthermore, reduced morbidity was observed for influenza virus-infected Trem1 −/− mice. Importantly, while immune-associated pathologies were significantly reduced, Trem1 −/− mice were equally capable of controlling infections with L. major , influenza virus, but also Legionella pneumophila as Trem1 +/+ controls. Our results not only demonstrate an unanticipated pathogenic impact of TREM-1 during a viral and parasitic infection, but also indicate that therapeutic blocking of TREM-1 in distinct inflammatory disorders holds considerable promise by blunting excessive inflammation while preserving the capacity for microbial control. Triggering receptor expressed on myeloid cells-1 (TREM-1) is an immune receptor expressed by myeloid cells that has the capacity to augment pro-inflammatory responses in the context of a microbial infection. While a TREM-1-amplified response likely serves the efficient clearance of pathogens, it also bears the potential to cause substantial tissue damage or even death. Hence, TREM-1 appears a possible therapeutic target for tempering deleterious host-pathogen interactions. However, in models of bacterial sepsis controversial findings have been obtained regarding the requirement of TREM-1 for bacterial control - depending on the overall degree of the TREM-1 blockade that was achieved. In order to conclusively investigate harmful versus essential functions of TREM-1 in vivo , we have generated mice deficient in Trem1 . Trem1 −/− mice were subjected to experimentally-induced intestinal inflammation (as a model of a non-infectious, yet microbial-driven disease) and also analysed following infections with Leishmania major , influenza virus and Legionella pneumophila . Across all models analysed, Trem1 −/− mice showed substantially reduced immune-associated disease. We thus describe a previously unanticipated pathogenic role for TREM-1 also during a parasitic and viral infection. Importantly, our data suggest that in certain diseases microbial control can be achieved in the context of blunted inflammation in the absence of TREM-1. |
| Audience | Academic |
| Author | Kaufmann, Thomas Tacchini-Cottier, Fabienne Oxenius, Annette Saurer, Leslie Schürch, Christian Riether, Carsten Schneider, Christoph Pawelski, Helga Schuster, Steffen Siegrist, Mark Kopf, Manfred Rihs, Silvia Mueller, Christoph Weber, Benjamin Genitsch, Vera Reith, Walter Dickgreber, Nina Zysset, Daniel Gurzeler, Ursina Ziltener, Pascal Ochsenbein, Adrian Hofstetter, Willy |
| AuthorAffiliation | 8 Department of Pathology and Immunology, Centre Medical Universitaire, Geneva, Switzerland University of California, Los Angeles, United States of America 4 Institute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland 2 Department of Biochemistry, University of Lausanne, Epalinges, Switzerland 5 Institute of Pharmacology, University of Bern, Bern, Switzerland 6 Institute of Microbiology, ETH Zurich, Zurich, Switzerland 3 Department of Clinical Research, University of Bern, Bern, Switzerland 1 Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland 7 Department of Medical Oncology, University of Bern, Bern, Switzerland |
| AuthorAffiliation_xml | – name: 5 Institute of Pharmacology, University of Bern, Bern, Switzerland – name: 2 Department of Biochemistry, University of Lausanne, Epalinges, Switzerland – name: 7 Department of Medical Oncology, University of Bern, Bern, Switzerland – name: 3 Department of Clinical Research, University of Bern, Bern, Switzerland – name: 4 Institute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland – name: 1 Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – name: 6 Institute of Microbiology, ETH Zurich, Zurich, Switzerland – name: 8 Department of Pathology and Immunology, Centre Medical Universitaire, Geneva, Switzerland – name: University of California, Los Angeles, United States of America |
| Author_xml | – sequence: 1 givenname: Benjamin surname: Weber fullname: Weber, Benjamin organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – sequence: 2 givenname: Steffen surname: Schuster fullname: Schuster, Steffen organization: Department of Biochemistry, University of Lausanne, Epalinges, Switzerland – sequence: 3 givenname: Daniel surname: Zysset fullname: Zysset, Daniel organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – sequence: 4 givenname: Silvia surname: Rihs fullname: Rihs, Silvia organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – sequence: 5 givenname: Nina surname: Dickgreber fullname: Dickgreber, Nina organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – sequence: 6 givenname: Christian surname: Schürch fullname: Schürch, Christian organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland ; Department of Clinical Research, University of Bern, Bern, Switzerland – sequence: 7 givenname: Carsten surname: Riether fullname: Riether, Carsten organization: Department of Clinical Research, University of Bern, Bern, Switzerland – sequence: 8 givenname: Mark surname: Siegrist fullname: Siegrist, Mark organization: Department of Clinical Research, University of Bern, Bern, Switzerland – sequence: 9 givenname: Christoph surname: Schneider fullname: Schneider, Christoph organization: Institute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland – sequence: 10 givenname: Helga surname: Pawelski fullname: Pawelski, Helga organization: Institute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland – sequence: 11 givenname: Ursina surname: Gurzeler fullname: Gurzeler, Ursina organization: Institute of Pharmacology, University of Bern, Bern, Switzerland – sequence: 12 givenname: Pascal surname: Ziltener fullname: Ziltener, Pascal organization: Institute of Microbiology, ETH Zurich, Zurich, Switzerland – sequence: 13 givenname: Vera surname: Genitsch fullname: Genitsch, Vera organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – sequence: 14 givenname: Fabienne surname: Tacchini-Cottier fullname: Tacchini-Cottier, Fabienne organization: Department of Biochemistry, University of Lausanne, Epalinges, Switzerland – sequence: 15 givenname: Adrian surname: Ochsenbein fullname: Ochsenbein, Adrian organization: Department of Clinical Research, University of Bern, Bern, Switzerland ; Department of Medical Oncology, University of Bern, Bern, Switzerland – sequence: 16 givenname: Willy surname: Hofstetter fullname: Hofstetter, Willy organization: Department of Clinical Research, University of Bern, Bern, Switzerland – sequence: 17 givenname: Manfred surname: Kopf fullname: Kopf, Manfred organization: Institute of Molecular Health Sciences, ETH Zurich, Zurich, Switzerland – sequence: 18 givenname: Thomas surname: Kaufmann fullname: Kaufmann, Thomas organization: Institute of Pharmacology, University of Bern, Bern, Switzerland – sequence: 19 givenname: Annette surname: Oxenius fullname: Oxenius, Annette organization: Institute of Microbiology, ETH Zurich, Zurich, Switzerland – sequence: 20 givenname: Walter surname: Reith fullname: Reith, Walter organization: Department of Pathology and Immunology, Centre Medical Universitaire, Geneva, Switzerland – sequence: 21 givenname: Leslie surname: Saurer fullname: Saurer, Leslie organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland – sequence: 22 givenname: Christoph surname: Mueller fullname: Mueller, Christoph organization: Division of Experimental Pathology, Institute of Pathology, University of Bern, Bern, Switzerland |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24453980$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2014 Public Library of Science 2014 Weber et al 2014 Weber et al 2014 Weber et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Weber B, Schuster S, Zysset D, Rihs S, Dickgreber N, et al. (2014) TREM-1 Deficiency Can Attenuate Disease Severity without Affecting Pathogen Clearance. PLoS Pathog 10(1): e1003900. doi:10.1371/journal.ppat.1003900 |
| Copyright_xml | – notice: COPYRIGHT 2014 Public Library of Science – notice: 2014 Weber et al 2014 Weber et al – notice: 2014 Weber et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Weber B, Schuster S, Zysset D, Rihs S, Dickgreber N, et al. (2014) TREM-1 Deficiency Can Attenuate Disease Severity without Affecting Pathogen Clearance. PLoS Pathog 10(1): e1003900. doi:10.1371/journal.ppat.1003900 |
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| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. Creative Commons Attribution License |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c699t-6c10aca96cdbf99c5f580533124ee286166bb224e19d0c8f76cb9e9e598fbf563 |
| Notes | Conceived and designed the experiments: BW SS CSchü CR MS CSchn HP UG PZ FTC AOc WH MK TK AOx WR LS CM. Performed the experiments: BW SS DZ SR ND CSchü CR MS CSchn HP UG PZ. Analyzed the data: BW SS DZ ND CSchü CR MS CSchn HP UG PZ VG FTC AOc WH MK TK AOc WR LS CM. Contributed reagents/materials/analysis tools: FTC WH MK TK AOc WR. Wrote the paper: LS CM. Obtained permission for use of the lentiviral Hoxb8 expression system and the CHO/mmSCF cells: TK. The authors have declared that no competing interests exist. |
| OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894224/ |
| PMID | 24453980 |
| ParticipantIDs | plos_journals_1498393060 doaj_primary_oai_doaj_org_article_42262ea844a64ff3b8f92dc971b3e0fb pubmedcentral_primary_oai_pubmedcentral_nih_gov_3894224 gale_infotracmisc_A364854398 gale_infotracacademiconefile_A364854398 gale_incontextgauss_ISR_A364854398 gale_incontextgauss_ISN_A364854398 crossref_primary_10_1371_journal_ppat_1003900 pubmed_primary_24453980 |
| PublicationCentury | 2000 |
| PublicationDate | 2014-01-01 |
| PublicationDateYYYYMMDD | 2014-01-01 |
| PublicationDate_xml | – month: 01 year: 2014 text: 2014-01-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: San Francisco, USA |
| PublicationTitle | PLoS pathogens |
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| Publisher | Public Library of Science Public Library of Science (PLoS) |
| Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
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| Snippet | Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses... Triggering receptor expressed on myeloid cells-1 (TREM-1) is a potent amplifier of pro-inflammatory innate immune reactions. While TREM-1-amplified responses... |
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| Title | TREM-1 deficiency can attenuate disease severity without affecting pathogen clearance |
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