Renal-associated TLR2 mediates ischemia/reperfusion injury in the kidney

TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA is mainly expressed by tubular cells and is enhanced upon renal ischemia/reperfusion (I/R) injury. We evaluated the role of TLR2 in I/R inju...

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Veröffentlicht in:	The Journal of clinical investigation Jg. 115; H. 10; S. 2894 - 2903
Hauptverfasser:	Leemans, Jaklien C., Stokman, Geurt, Claessen, Nike, Rouschop, Kasper M., Teske, Gwendoline J.D., Kirschning, Carsten J., Akira, Shizuo, van der Poll, Tom, Weening, Jan J., Florquin, Sandrine
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States American Society for Clinical Investigation 01.10.2005
Schlagworte:	Adaptive immunity Animals Antigens Biomedical research Cells, Cultured Chemokines Chemokines - immunology Chimera - genetics Chimera - immunology Cytokines Inflammation Inflammation - genetics Inflammation - immunology Inflammation - pathology Inflammation - prevention & control Ischemia Kidney Diseases - genetics Kidney Diseases - immunology Kidney Diseases - pathology Kidney Diseases - prevention & control Kidney Tubules - immunology Kidney Tubules - pathology Kidneys Leukocytes Leukocytes - immunology Male Mice Mice, Knockout Oligodeoxyribonucleotides, Antisense - immunology Oligodeoxyribonucleotides, Antisense - pharmacology Oligodeoxyribonucleotides, Antisense - therapeutic use Pathogens Proteins Reperfusion Injury - genetics Reperfusion Injury - immunology Reperfusion Injury - pathology Reperfusion Injury - prevention & control Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - immunology
ISSN:	0021-9738, 1558-8238
Online-Zugang:	Volltext
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Abstract	TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA is mainly expressed by tubular cells and is enhanced upon renal ischemia/reperfusion (I/R) injury. We evaluated the role of TLR2 in I/R injury using TLR2-/- and TLR2+/+ mice, TLR2 antisense oligonucleotides, and chimeric mice deficient in leukocyte or renal TLR2. Tubular cells needed TLR2 to produce significant cytokine and chemokine amounts upon ischemia in vitro. TLR2 played a proinflammatory and detrimental role in vivo after I/R injury, as reflected by a reduction in the amount of local cytokines and chemokines, leukocytes, and the level of renal injury and dysfunction in TLR2-/- mice compared with controls. Analysis of chimeric mice suggested that TLR2 expressed on renal parenchyma plays a crucial role in the induction of inflammation and injury. TLR2-antisense treatment protected mice from renal dysfunction, neutrophil influx, and tubular apoptosis after I/R injury compared with nonsense treatment. In summary, we identified renal-associated TLR2 as an important initiator of inflammatory responses leading to renal injury and dysfunction in I/R injury. These data imply that TLR2 blockade could provide a basis for therapeutic strategies to treat or prevent renal ischemic injury.
AbstractList	TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA is mainly expressed by tubular cells and is enhanced upon renal ischemia/reperfusion (I/R) injury. We evaluated the role of TLR2 in I/R injury using TLR2–/– and TLR2+/+ mice, TLR2 antisense oligonucleotides, and chimeric mice deficient in leukocyte or renal TLR2. Tubular cells needed TLR2 to produce significant cytokine and chemokine amounts upon ischemia in vitro. TLR2 played a proinflammatory and detrimental role in vivo after I/R injury, as reflected by a reduction in the amount of local cytokines and chemokines, leukocytes, and the level of renal injury and dysfunction in TLR2–/– mice compared with controls. Analysis of chimeric mice suggested that TLR2 expressed on renal parenchyma plays a crucial role in the induction of inflammation and injury. TLR2-antisense treatment protected mice from renal dysfunction, neutrophil influx, and tubular apoptosis after I/R injury compared with nonsense treatment. In summary, we identified renal-associated TLR2 as an important initiator of inflammatory responses leading to renal injury and dysfunction in I/R injury. These data imply that TLR2 blockade could provide a basis for therapeutic strategies to treat or prevent renal ischemic injury. TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA is mainly expressed by tubular cells and is enhanced upon renal ischemia/reperfusion (I/R) injury. We evaluated the role of TLR2 in I/R injury using TLR2-/- and TLR2+/+ mice, TLR2 antisense oligonucleotides, and chimeric mice deficient in leukocyte or renal TLR2. Tubular cells needed TLR2 to produce significant cytokine and chemokine amounts upon ischemia in vitro. TLR2 played a proinflammatory and detrimental role in vivo after I/R injury, as reflected by a reduction in the amount of local cytokines and chemokines, leukocytes, and the level of renal injury and dysfunction in TLR2-/- mice compared with controls. Analysis of chimeric mice suggested that TLR2 expressed on renal parenchyma plays a crucial role in the induction of inflammation and injury. TLR2-antisense treatment protected mice from renal dysfunction, neutrophil influx, and tubular apoptosis after I/R injury compared with nonsense treatment. In summary, we identified renal-associated TLR2 as an important initiator of inflammatory responses leading to renal injury and dysfunction in I/R injury. These data imply that TLR2 blockade could provide a basis for therapeutic strategies to treat or prevent renal ischemic injury.TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA is mainly expressed by tubular cells and is enhanced upon renal ischemia/reperfusion (I/R) injury. We evaluated the role of TLR2 in I/R injury using TLR2-/- and TLR2+/+ mice, TLR2 antisense oligonucleotides, and chimeric mice deficient in leukocyte or renal TLR2. Tubular cells needed TLR2 to produce significant cytokine and chemokine amounts upon ischemia in vitro. TLR2 played a proinflammatory and detrimental role in vivo after I/R injury, as reflected by a reduction in the amount of local cytokines and chemokines, leukocytes, and the level of renal injury and dysfunction in TLR2-/- mice compared with controls. Analysis of chimeric mice suggested that TLR2 expressed on renal parenchyma plays a crucial role in the induction of inflammation and injury. TLR2-antisense treatment protected mice from renal dysfunction, neutrophil influx, and tubular apoptosis after I/R injury compared with nonsense treatment. In summary, we identified renal-associated TLR2 as an important initiator of inflammatory responses leading to renal injury and dysfunction in I/R injury. These data imply that TLR2 blockade could provide a basis for therapeutic strategies to treat or prevent renal ischemic injury.
Author	Weening, Jan J. Stokman, Geurt Claessen, Nike Rouschop, Kasper M. Teske, Gwendoline J.D. van der Poll, Tom Florquin, Sandrine Kirschning, Carsten J. Leemans, Jaklien C. Akira, Shizuo
AuthorAffiliation	1 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. 2 Institute of Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Munich, Germany. 3 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan. 4 Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
AuthorAffiliation_xml	– name: 1 Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. 2 Institute of Medical Microbiology, Immunology, and Hygiene, Technical University of Munich, Munich, Germany. 3 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan. 4 Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Author_xml	– sequence: 1 givenname: Jaklien C. surname: Leemans fullname: Leemans, Jaklien C. – sequence: 2 givenname: Geurt surname: Stokman fullname: Stokman, Geurt – sequence: 3 givenname: Nike surname: Claessen fullname: Claessen, Nike – sequence: 4 givenname: Kasper M. surname: Rouschop fullname: Rouschop, Kasper M. – sequence: 5 givenname: Gwendoline J.D. surname: Teske fullname: Teske, Gwendoline J.D. – sequence: 6 givenname: Carsten J. surname: Kirschning fullname: Kirschning, Carsten J. – sequence: 7 givenname: Shizuo surname: Akira fullname: Akira, Shizuo – sequence: 8 givenname: Tom surname: van der Poll fullname: van der Poll, Tom – sequence: 9 givenname: Jan J. surname: Weening fullname: Weening, Jan J. – sequence: 10 givenname: Sandrine surname: Florquin fullname: Florquin, Sandrine
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/16167081$$D View this record in MEDLINE/PubMed
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Snippet	TLRs are conserved pattern recognition receptors that detect motifs of pathogens and host material released during injury. For unknown reasons, renal TLR2 mRNA...
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SubjectTerms	Adaptive immunity Animals Antigens Biomedical research Cells, Cultured Chemokines Chemokines - immunology Chimera - genetics Chimera - immunology Cytokines Inflammation Inflammation - genetics Inflammation - immunology Inflammation - pathology Inflammation - prevention & control Ischemia Kidney Diseases - genetics Kidney Diseases - immunology Kidney Diseases - pathology Kidney Diseases - prevention & control Kidney Tubules - immunology Kidney Tubules - pathology Kidneys Leukocytes Leukocytes - immunology Male Mice Mice, Knockout Oligodeoxyribonucleotides, Antisense - immunology Oligodeoxyribonucleotides, Antisense - pharmacology Oligodeoxyribonucleotides, Antisense - therapeutic use Pathogens Proteins Reperfusion Injury - genetics Reperfusion Injury - immunology Reperfusion Injury - pathology Reperfusion Injury - prevention & control Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - immunology
Title	Renal-associated TLR2 mediates ischemia/reperfusion injury in the kidney
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