Thirty-Eight-Negative Kinase 1 Is a Mediator of Acute Kidney Injury in Experimental and Clinical Traumatic Hemorrhagic Shock
Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patie...
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| Published in | Frontiers in immunology Vol. 11; p. 2081 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Switzerland
Frontiers Media S.A
26.08.2020
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| Abstract | Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patient at great risk for adverse outcome. Recently, thirty-eight-negative kinase 1 (TNK1) was proposed to play a detrimental role in organ damage after trauma/HS. Therefore, we aimed to assess the role of TNK1 in HS-induced kidney injury in a murine and a
analysis of a non-human primate model of HS comparable to the clinical situation. Mice and non-human primates underwent resuscitated HS at 30 mmHg for 60 min. 5 h after the induction of shock, animals were assessed for systemic inflammation and TNK1 expression in the kidney.
, murine distal convoluted tubule cells were stimulated with inflammatory mediators to gain mechanistic insights into the role of TNK1 in kidney dysfunction. In a translational approach, we investigated blood drawn from either healthy volunteers or severely injured patients at different time points after trauma (from arrival at the emergency room and at fixed time intervals until 10 days post injury; identifier: NCT02682550, https://clinicaltrials.gov/ct2/show/NCT02682550). A pronounced inflammatory response, as seen by increased IL-6 plasma levels as well as early signs of AKI, were observed in mice, non-human primates, and humans after trauma/HS. TNK1 was found in the plasma early after trauma-HS in trauma patients. Renal TNK1 expression was significantly increased in mice and non-human primates after HS, and these effects with concomitant induction of apoptosis were blocked by therapeutic inhibition of complement C3 activation in non-human primates. Mechanistically,
data suggested that IL-6 rather than C3 cleavage products induced upregulation of TNK1 and impaired barrier function in renal epithelial cells. In conclusion, these data indicate that C3 inhibition
may inhibit an excessive inflammatory response and mediator release, thereby indirectly neutralizing TNK1 as a potent driver of organ damage. In future studies, we will address the therapeutic potential of direct TNK1 inhibition in the context of severe tissue trauma with different degrees of additional HS. |
|---|---|
| AbstractList | Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patient at great risk for adverse outcome. Recently, thirty-eight-negative kinase 1 (TNK1) was proposed to play a detrimental role in organ damage after trauma/HS. Therefore, we aimed to assess the role of TNK1 in HS-induced kidney injury in a murine and apost hocanalysis of a non-human primate model of HS comparable to the clinical situation. Mice and non-human primates underwent resuscitated HS at 30 mmHg for 60 min. 5 h after the induction of shock, animals were assessed for systemic inflammation and TNK1 expression in the kidney.In vitro, murine distal convoluted tubule cells were stimulated with inflammatory mediators to gain mechanistic insights into the role of TNK1 in kidney dysfunction. In a translational approach, we investigated blood drawn from either healthy volunteers or severely injured patients at different time points after trauma (from arrival at the emergency room and at fixed time intervals until 10 days post injury; identifier: NCT02682550,). A pronounced inflammatory response, as seen by increased IL-6 plasma levels as well as early signs of AKI, were observed in mice, non-human primates, and humans after trauma/HS. TNK1 was found in the plasma early after trauma-HS in trauma patients. Renal TNK1 expression was significantly increased in mice and non-human primates after HS, and these effects with concomitant induction of apoptosis were blocked by therapeutic inhibition of complement C3 activation in non-human primates. Mechanistically,in vitrodata suggested that IL-6 rather than C3 cleavage products induced upregulation of TNK1 and impaired barrier function in renal epithelial cells. In conclusion, these data indicate that C3 inhibitionin vivomay inhibit an excessive inflammatory response and mediator release, thereby indirectly neutralizing TNK1 as a potent driver of organ damage. In future studies, we will address the therapeutic potential of direct TNK1 inhibition in the context of severe tissue trauma with different degrees of additional HS. Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patient at great risk for adverse outcome. Recently, thirty-eight-negative kinase 1 (TNK1) was proposed to play a detrimental role in organ damage after trauma/HS. Therefore, we aimed to assess the role of TNK1 in HS-induced kidney injury in a murine and a post hoc analysis of a non-human primate model of HS comparable to the clinical situation. Mice and non-human primates underwent resuscitated HS at 30 mmHg for 60 min. 5 h after the induction of shock, animals were assessed for systemic inflammation and TNK1 expression in the kidney. In vitro , murine distal convoluted tubule cells were stimulated with inflammatory mediators to gain mechanistic insights into the role of TNK1 in kidney dysfunction. In a translational approach, we investigated blood drawn from either healthy volunteers or severely injured patients at different time points after trauma (from arrival at the emergency room and at fixed time intervals until 10 days post injury; identifier: NCT02682550, https://clinicaltrials.gov/ct2/show/NCT02682550 ). A pronounced inflammatory response, as seen by increased IL-6 plasma levels as well as early signs of AKI, were observed in mice, non-human primates, and humans after trauma/HS. TNK1 was found in the plasma early after trauma-HS in trauma patients. Renal TNK1 expression was significantly increased in mice and non-human primates after HS, and these effects with concomitant induction of apoptosis were blocked by therapeutic inhibition of complement C3 activation in non-human primates. Mechanistically, in vitro data suggested that IL-6 rather than C3 cleavage products induced upregulation of TNK1 and impaired barrier function in renal epithelial cells. In conclusion, these data indicate that C3 inhibition in vivo may inhibit an excessive inflammatory response and mediator release, thereby indirectly neutralizing TNK1 as a potent driver of organ damage. In future studies, we will address the therapeutic potential of direct TNK1 inhibition in the context of severe tissue trauma with different degrees of additional HS. Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patient at great risk for adverse outcome. Recently, thirty-eight-negative kinase 1 (TNK1) was proposed to play a detrimental role in organ damage after trauma/HS. Therefore, we aimed to assess the role of TNK1 in HS-induced kidney injury in a murine and a analysis of a non-human primate model of HS comparable to the clinical situation. Mice and non-human primates underwent resuscitated HS at 30 mmHg for 60 min. 5 h after the induction of shock, animals were assessed for systemic inflammation and TNK1 expression in the kidney. , murine distal convoluted tubule cells were stimulated with inflammatory mediators to gain mechanistic insights into the role of TNK1 in kidney dysfunction. In a translational approach, we investigated blood drawn from either healthy volunteers or severely injured patients at different time points after trauma (from arrival at the emergency room and at fixed time intervals until 10 days post injury; identifier: NCT02682550, https://clinicaltrials.gov/ct2/show/NCT02682550). A pronounced inflammatory response, as seen by increased IL-6 plasma levels as well as early signs of AKI, were observed in mice, non-human primates, and humans after trauma/HS. TNK1 was found in the plasma early after trauma-HS in trauma patients. Renal TNK1 expression was significantly increased in mice and non-human primates after HS, and these effects with concomitant induction of apoptosis were blocked by therapeutic inhibition of complement C3 activation in non-human primates. Mechanistically, data suggested that IL-6 rather than C3 cleavage products induced upregulation of TNK1 and impaired barrier function in renal epithelial cells. In conclusion, these data indicate that C3 inhibition may inhibit an excessive inflammatory response and mediator release, thereby indirectly neutralizing TNK1 as a potent driver of organ damage. In future studies, we will address the therapeutic potential of direct TNK1 inhibition in the context of severe tissue trauma with different degrees of additional HS. Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of systemic inflammation and organ damage. The kidney is often strongly affected by traumatic-HS, and acute kidney injury (AKI) poses the patient at great risk for adverse outcome. Recently, thirty-eight-negative kinase 1 (TNK1) was proposed to play a detrimental role in organ damage after trauma/HS. Therefore, we aimed to assess the role of TNK1 in HS-induced kidney injury in a murine and a post hoc analysis of a non-human primate model of HS comparable to the clinical situation. Mice and non-human primates underwent resuscitated HS at 30 mmHg for 60 min. 5 h after the induction of shock, animals were assessed for systemic inflammation and TNK1 expression in the kidney. In vitro, murine distal convoluted tubule cells were stimulated with inflammatory mediators to gain mechanistic insights into the role of TNK1 in kidney dysfunction. In a translational approach, we investigated blood drawn from either healthy volunteers or severely injured patients at different time points after trauma (from arrival at the emergency room and at fixed time intervals until 10 days post injury; identifier: NCT02682550, https://clinicaltrials.gov/ct2/show/NCT02682550). A pronounced inflammatory response, as seen by increased IL-6 plasma levels as well as early signs of AKI, were observed in mice, non-human primates, and humans after trauma/HS. TNK1 was found in the plasma early after trauma-HS in trauma patients. Renal TNK1 expression was significantly increased in mice and non-human primates after HS, and these effects with concomitant induction of apoptosis were blocked by therapeutic inhibition of complement C3 activation in non-human primates. Mechanistically, in vitro data suggested that IL-6 rather than C3 cleavage products induced upregulation of TNK1 and impaired barrier function in renal epithelial cells. In conclusion, these data indicate that C3 inhibition in vivo may inhibit an excessive inflammatory response and mediator release, thereby indirectly neutralizing TNK1 as a potent driver of organ damage. In future studies, we will address the therapeutic potential of direct TNK1 inhibition in the context of severe tissue trauma with different degrees of additional HS. |
| Author | Radermacher, Peter Seufferlein, Thomas van Griensven, Martijn Halbgebauer, Rebecca Eigner, Alica Resuello, Ranillo R G Palmer, Annette Schäfer, Fabian Wachter, Ulrich Braun, Christian K Tuplano, Joel V Kleger, Alexander Braumüller, Sonja Nilsson Ekdahl, Kristina Lambris, John D Bückle, Sarah Gebhard, Florian Karasu, Ebru Schultze, Anke Armacki, Milena Nilsson, Bo Kalbitz, Miriam Huber-Lang, Markus |
| AuthorAffiliation | 5 Department of Immunology, Genetics and Pathology, Uppsala University , Uppsala , Sweden 6 Centre of Biomaterials Chemistry, Linnaeus University , Kalmar , Sweden 3 Institute for Anesthesiological Pathophysiology and Process Development, University of Ulm , Ulm , Germany 4 Simian Conservation Breeding and Research Center , Makati , Philippines 2 Department of Pediatrics and Adolescent Medicine, University Hospital Ulm , Ulm , Germany 9 Department of Pathology and Laboratory Medicine, University of Pennsylvania , Philadelphia, PA , United States 8 Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University Hospital Ulm , Ulm , Germany 7 Department of Internal Medicine I, University Hospital Ulm , Ulm , Germany 1 Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm , Ulm , Germany 10 MERLN Institute for Technology-Inspired Regenerative Medicine, Department of Cell Biology-Inspired Tissue Engineering, Maastricht University , |
| AuthorAffiliation_xml | – name: 3 Institute for Anesthesiological Pathophysiology and Process Development, University of Ulm , Ulm , Germany – name: 10 MERLN Institute for Technology-Inspired Regenerative Medicine, Department of Cell Biology-Inspired Tissue Engineering, Maastricht University , Maastricht , Netherlands – name: 8 Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University Hospital Ulm , Ulm , Germany – name: 1 Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm , Ulm , Germany – name: 2 Department of Pediatrics and Adolescent Medicine, University Hospital Ulm , Ulm , Germany – name: 4 Simian Conservation Breeding and Research Center , Makati , Philippines – name: 5 Department of Immunology, Genetics and Pathology, Uppsala University , Uppsala , Sweden – name: 6 Centre of Biomaterials Chemistry, Linnaeus University , Kalmar , Sweden – name: 9 Department of Pathology and Laboratory Medicine, University of Pennsylvania , Philadelphia, PA , United States – name: 7 Department of Internal Medicine I, University Hospital Ulm , Ulm , Germany |
| Author_xml | – sequence: 1 givenname: Rebecca surname: Halbgebauer fullname: Halbgebauer, Rebecca organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 2 givenname: Ebru surname: Karasu fullname: Karasu, Ebru organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 3 givenname: Christian K surname: Braun fullname: Braun, Christian K organization: Department of Pediatrics and Adolescent Medicine, University Hospital Ulm, Ulm, Germany – sequence: 4 givenname: Annette surname: Palmer fullname: Palmer, Annette organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 5 givenname: Sonja surname: Braumüller fullname: Braumüller, Sonja organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 6 givenname: Anke surname: Schultze fullname: Schultze, Anke organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 7 givenname: Fabian surname: Schäfer fullname: Schäfer, Fabian organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 8 givenname: Sarah surname: Bückle fullname: Bückle, Sarah organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 9 givenname: Alica surname: Eigner fullname: Eigner, Alica organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany – sequence: 10 givenname: Ulrich surname: Wachter fullname: Wachter, Ulrich organization: Institute for Anesthesiological Pathophysiology and Process Development, University of Ulm, Ulm, Germany – sequence: 11 givenname: Peter surname: Radermacher fullname: Radermacher, Peter organization: Institute for Anesthesiological Pathophysiology and Process Development, University of Ulm, Ulm, Germany – sequence: 12 givenname: Ranillo R G surname: Resuello fullname: Resuello, Ranillo R G organization: Simian Conservation Breeding and Research Center, Makati, Philippines – sequence: 13 givenname: Joel V surname: Tuplano fullname: Tuplano, Joel V organization: Simian Conservation Breeding and Research Center, Makati, Philippines – sequence: 14 givenname: Kristina surname: Nilsson Ekdahl fullname: Nilsson Ekdahl, Kristina organization: Centre of Biomaterials Chemistry, Linnaeus University, Kalmar, Sweden – sequence: 15 givenname: Bo surname: Nilsson fullname: Nilsson, Bo organization: Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden – sequence: 16 givenname: Milena surname: Armacki fullname: Armacki, Milena organization: Department of Internal Medicine I, University Hospital Ulm, Ulm, Germany – sequence: 17 givenname: Alexander surname: Kleger fullname: Kleger, Alexander organization: Department of Internal Medicine I, University Hospital Ulm, Ulm, Germany – sequence: 18 givenname: Thomas surname: Seufferlein fullname: Seufferlein, Thomas organization: Department of Internal Medicine I, University Hospital Ulm, Ulm, Germany – sequence: 19 givenname: Miriam surname: Kalbitz fullname: Kalbitz, Miriam organization: Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University Hospital Ulm, Ulm, Germany – sequence: 20 givenname: Florian surname: Gebhard fullname: Gebhard, Florian organization: Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, Center of Surgery, University Hospital Ulm, Ulm, Germany – sequence: 21 givenname: John D surname: Lambris fullname: Lambris, John D organization: Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA, United States – sequence: 22 givenname: Martijn surname: van Griensven fullname: van Griensven, Martijn organization: MERLN Institute for Technology-Inspired Regenerative Medicine, Department of Cell Biology-Inspired Tissue Engineering, Maastricht University, Maastricht, Netherlands – sequence: 23 givenname: Markus surname: Huber-Lang fullname: Huber-Lang, Markus organization: Institute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany |
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| Copyright | Copyright © 2020 Halbgebauer, Karasu, Braun, Palmer, Braumüller, Schultze, Schäfer, Bückle, Eigner, Wachter, Radermacher, Resuello, Tuplano, Nilsson Ekdahl, Nilsson, Armacki, Kleger, Seufferlein, Kalbitz, Gebhard, Lambris, van Griensven and Huber-Lang. Copyright © 2020 Halbgebauer, Karasu, Braun, Palmer, Braumüller, Schultze, Schäfer, Bückle, Eigner, Wachter, Radermacher, Resuello, Tuplano, Nilsson Ekdahl, Nilsson, Armacki, Kleger, Seufferlein, Kalbitz, Gebhard, Lambris, van Griensven and Huber-Lang. 2020 Halbgebauer, Karasu, Braun, Palmer, Braumüller, Schultze, Schäfer, Bückle, Eigner, Wachter, Radermacher, Resuello, Tuplano, Nilsson Ekdahl, Nilsson, Armacki, Kleger, Seufferlein, Kalbitz, Gebhard, Lambris, van Griensven and Huber-Lang |
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| Keywords | trauma blood loss inflammation TNK1 injury complement IL-6 AKI |
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| License | Copyright © 2020 Halbgebauer, Karasu, Braun, Palmer, Braumüller, Schultze, Schäfer, Bückle, Eigner, Wachter, Radermacher, Resuello, Tuplano, Nilsson Ekdahl, Nilsson, Armacki, Kleger, Seufferlein, Kalbitz, Gebhard, Lambris, van Griensven and Huber-Lang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 Edited by: Guochang Hu, University of Illinois at Chicago, United States This article was submitted to Inflammation, a section of the journal Frontiers in Immunology Reviewed by: Yongqing Li, University of Michigan, United States; Hernando Gomez, University of Pittsburgh, United States |
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| Snippet | Trauma represents a major socioeconomic burden worldwide. After a severe injury, hemorrhagic shock (HS) as a frequent concomitant aspect is a central driver of... |
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| SubjectTerms | Acute Kidney Injury AKI Animals blood loss Cells, Cultured complement Complement C3 - metabolism Fetal Proteins - genetics Fetal Proteins - metabolism Healthy Volunteers Humans IL-6 Immunologi Immunology inflammation Inflammation Mediators - metabolism injury Interleukin-6 - metabolism Kidney Male Mice Mice, Inbred C57BL Models, Animal Primates Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Shock, Hemorrhagic - metabolism TNK1 trauma Wounds and Injuries - metabolism |
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| Title | Thirty-Eight-Negative Kinase 1 Is a Mediator of Acute Kidney Injury in Experimental and Clinical Traumatic Hemorrhagic Shock |
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