Collaborative Research Center 1149

Danger Response, Disturbance Factors and Regenerative Potential after Acute Trauma

Trauma as a mechanical injury to tissue affects a vast number of people worldwide at any time throughout their life. The trauma-triggered acute danger response induces potent regeneration and healing processes. However, significant complications, including systemic inflammation and organ dysfunction, may develop post trauma, particularly in the presence of numerous disturbance factors (e.g. co-morbidities). The underlying pathophysiological mechanisms are complex and currently poorly understood. Furthermore, clinical trauma management on all levels requires early recognition and pathophysiological understanding of the trauma reaction and deduction of effective individualised therapeutic strategies.

Focusing on the most common injury patterns, major disturbance factors, and regenerative mechanisms, the proposed Collaborative Research Centre (CRC) 1149 at Ulm University aims to provide profound pathomechanistic understanding of the systemic and local cellular and molecular trauma responses and related complications for transfer into effective therapeutic trauma strategies.

Several unique features of the centre will facilitate realisation of the integrative and translational approach; these include a cross-disciplinary and highly collaborative scientific environment within the zmfu (Centre of Musculoskeletal Research Ulm), the Clinical Research Unit KFO200 and the Trans-regional Research Unit 793, and the long-standing commitment of the Medical Faculty at Ulm University to cutting-edge basic, (re)translational, and clinical research in trauma. These attributes are complemented by sophisticated, clinically relevant in vitro and in vivo models of the trauma impact and resulting complications to gain deep insights into the mechanistic complexity and regeneration potential post trauma as well as to evaluate innovative cell- and molecular based therapies.

As compelling scientific and clinical challenges, central hypotheses are defined in the CRC, proposing to:

A) better understand the danger response after trauma on a molecular, cellular, organ, and organism level;

B) determine the influence of major disturbance factors (co-morbidities) on the trauma response;

C) define mechanisms of the dysfunction and potential of regeneration post trauma and adapt them to trauma management.

These central hypotheses are reflected by three project groups (A, B, and C) that will closely interact with each other, combining excellent basic research with clinical expertise:

Research group A will investigate the acute pro- and anti-inflammatory danger response after trauma including early cellular and molecular danger sensing, -translation, -clearance and -escalation mechanisms. This group of projects focuses on danger-associated molecular patterns (DAMPs) and their consequences on early organ-blood barrier failure, synaptic (re)modelling, key inflammatory pathways (including NF-κB), and changes of the first line of cellular defence. 

In close collaboration, research group B will address the modulation and perturbation of the posttraumatic response by the most relevant co-morbidities (e.g. atherosclerosis, chronic obstructive pulmonary disease, and obesity) and substance abuse (e.g. nicotine and alcohol), and, furthermore, will identify long-term effects of multiple personal factors (e.g. age) in regard to healing processes in humans.

Furthering perceptions of project groups A and B, research group C pursues “resolving mechanisms” of the posttraumatic inflammatory response and the regenerative capacity, focusing on the role of pro- and antiinflammatory mediators (e.g. IL-6, corticosteroids) in tissue regeneration, and defining mobilisation/homing  mechanisms and the therapeutic potential of stem cells to improve healing processes after severe trauma.

For future-oriented avenues, early pro-regenerative responses will be investigated to generate new hypotheses and novel strategic thinking to fully restore tissue defects. In the long-term perspective, a valid functional immune monitoring of the individual danger response on the background of various co-morbidities and adapted immune- and cell-based therapies, for example by complement intervention and large-scale GMPgrade cellular ex vivo expansion, are anticipated.

Finally, the proposed CRC provides a superb opportunity to closer define and realise the concept of (re)translational research “from bedside to bench and back” for the danger response after tissue trauma. This approach will substantially contribute to a better understanding of trauma pathophysiology under “reallife” conditions, and, importantly, to an improved clinical management and outcome for trauma patients.

CRC 1149 Movie

Selected publications

  1. Rapp, A. E., Y. Hachemi, J. Kemmler, M. Koenen, J. Tuckermann et al., 2018 (2017 in press) Induced global deletion of glucocorticoid receptor impairs fracture healing. FASEB J.
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  3. Wiesner, D., L. Tar, B. Linkus, A. Chandrasekar, F. Olde Heuvel et al., 2018 Reversible induction of TDP-43 granules in cortical neurons after traumatic injury. Exp Neurol 299: 15-25.
  4. Denk, S., S. Weckbach, P. Eisele, C. K. Braun, R. Wiegner et al., 2018 Role of Hemorrhagic Shock in Experimental Polytrauma. Shock 49: 154-163.
  5. Amann, E. M., M. T. Rojewski, S. Rodi, D. Fürst, J. Fiedler et al., 2018 Systemic recovery and therapeutic effects of transplanted allogenic and xenogenic mesenchymal stromal cells in a rat blunt chest trauma model, pp. 218-231 in Cytotherapy.
  6. Zimprich, A., G. Mroz, C. Meyer Zu Reckendorf, S. Anastasiadou, P. Forstner et al., 2017 Serum Response Factor (SRF) Ablation Interferes with Acute Stress-Associated Immediate and Long-Term Coping Mechanisms. Mol Neurobiol 54: 8242-8262.
  7. Wrba, L., A. Palmer, C. K. Braun and M. Huber-Lang, 2017 Evaluation of gut-blood barrier dysfunction in various models of trauma, hemorrhagic shock, and burn injury. J Trauma Acute Care Surg 83: 944-953.
  8. Wehner, D., T. M. Tsarouchas, A. Michael, C. Haase, G. Weidinger et al., 2017 Wnt signaling controls pro-regenerative Collagen XII in functional spinal cord regeneration in zebrafish. Nat Commun 8: 126.
  9. Wanner, R., M. Gey, A. Abaei, D. Warnecke, L. de Roy et al., 2017 Functional and Molecular Characterization of a Novel Traumatic Peripheral Nerve-Muscle Injury Model. Neuromolecular Med 19: 357-374.
  10. Thielecke, L., T. Aranyossy, A. Dahl, R. Tiwari, I. Roeder et al., 2017 Limitations and challenges of genetic barcode quantification. Sci Rep 7: 43249.
  11. Singh, K., L. Krug, A. Basu, P. Meyer, N. Treiber et al., 2017 Alpha-Ketoglutarate Curbs Differentiation and Induces Cell Death in Mesenchymal Stromal Precursors with Mitochondrial Dysfunction. Stem Cells 35: 1704-1718.
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  32. Hartmann, C., P. Radermacher, M. Wepler and B. Nubaum, 2017 Non-Hemodynamic Effects of Catecholamines. Shock.
  33. Hartmann, C., M. Loconte, E. Antonucci, M. Holzhauser, T. Holle et al., 2017 Effects of Hyperoxia During Resuscitation From Hemorrhagic Shock in Swine With Preexisting Coronary Artery Disease. Crit Care Med 45: e1270-e1279.
  34. Hartmann, C., S. Hafner, A. Scheuerle, P. Moller, M. Huber-Lang et al., 2017 The Role of Cystathionine-gamma-Lyase In Blunt Chest Trauma in Cigarette Smoke Exposed Mice. Shock 47: 491-499.
  35. Halbgebauer, R., C. K. Braun, S. Denk, B. Mayer, P. Cinelli et al., 2017 Hemorrhagic shock drives glycocalyx, barrier and organ dysfunction early after polytrauma. J Crit Care 44: 229-237.
  36. Hagemeyer, N., K. M. Hanft, M. A. Akriditou, N. Unger, E. S. Park et al., 2017 Microglia contribute to normal myelinogenesis and to oligodendrocyte progenitor maintenance during adulthood. Acta Neuropathol 134: 441-458.
  37. Hafner, S., K. Wagner, S. Weber, M. Groger, M. Wepler et al., 2017 Role of the Purinergic Receptor P2XR4 After Blunt Chest Trauma in Cigarette Smoke-Exposed Mice. Shock 47: 193-199.
  38. Haffner-Luntzer, M., F. Muller-Graf, R. Matthys, Y. Hägele, V. Fischer et al., 2017 Evaluation of high-resolution In Vivo MRI for longitudinal analysis of endochondral fracture healing in mice. PLoS One 12: e0174283.
  39. Haffner-Luntzer, M., F. Müller-Graf, R. Matthys, A. Abaei, R. Jonas et al., 2017 In Vivo Evaluation of Fracture Callus Development During Bone Healing in Mice Using an MRI-compatible Osteosynthesis Device for the Mouse Femur. J Vis Exp: e56679.
  40. Haffner-Luntzer, M., V. Fischer, K. Prystaz, A. Liedert and A. Ignatius, 2017 The inflammatory phase of fracture healing is influenced by oestrogen status in mice. Eur J Med Res 33: 23.
  41. Guidi, N., M. Sacma, L. Standker, K. Soller, G. Marka et al., 2017 Osteopontin attenuates aging-associated phenotypes of hematopoietic stem cells. EMBO J 36: 1463.
  42. Gačanin, J., A. Kovtun, S. Fischer, V. Schwager, J. Quambusch et al., 2017 Spatiotemporally Controlled Release of Rho-Inhibiting C3 Toxin from a Protein–DNA Hybrid Hydrogel for Targeted Inhibition of Osteoclast Formation and Activity. Adv Healthc Mater 6: 1700392.
  43. Fois, G., V. E. Winkelmann, L. Bareis, L. Staudenmaier, E. Hecht et al., 2017 ATP is stored in lamellar bodies to activate vesicular P2X4 in an autocrine fashion upon exocytosis. J Gen Physiol.
  44. Foertsch, S., M. Haffner-Luntzer, J. Kroner, F. Gross, K. Kaiser et al., 2017 Chronic psychosocial stress disturbs long-bone growth in adolescent mice. Dis Model Mech 10: 1399-1409.
  45. Foertsch, S., A. M. Fuchsl, S. D. Faller, H. Holzer, D. Langgartner et al., 2017 Splenic glucocorticoid resistance following psychosocial stress requires physical injury. Sci Rep 7: 15730.
  46. Fattahi, F., M. Kalbitz, E. A. Malan, E. Abe, L. Jajou et al., 2017 Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction. FASEB J 31: 4129-4139.
  47. Ernst, K., J. Schmid, M. Beck, M. Hagele, M. Hohwieler et al., 2017 Hsp70 facilitates trans-membrane transport of bacterial ADP-ribosylating toxins into the cytosol of mammalian cells. Sci Rep 7: 2724.
  48. Denk, S., R. P. Taylor, R. Wiegner, E. M. Cook, M. A. Lindorfer et al., 2017 Complement C5a-Induced Changes in Neutrophil Morphology During Inflammation. Scand J Immunol 86: 143-155.
  49. Denk, S., M. D. Neher, D. A. C. Messerer, R. Wiegner, B. Nilsson et al., 2017 Complement C5a Functions as a Master Switch for the pH Balance in Neutrophils Exerting Fundamental Immunometabolic Effects. J Immunol 198: 4846-4854.
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  51. Chandrasekar, A., F. O. Heuvel, A. Palmer, B. Linkus, A. C. Ludolph et al., 2017 Acute ethanol administration results in a protective cytokine and neuroinflammatory profile in traumatic brain injury. Int Immunopharmacol 51: 66-75.
  52. Braun, C. K., M. Kalbitz, R. Halbgebauer, P. Eisele, D. A. C. Messerer et al., 2017 Early structural changes of the heart after experimental polytrauma and hemorrhagic shock. PLoS One 12: e0187327.
  53. Bonfanti, E., P. Gelosa, M. Fumagalli, L. Dimou, F. Vigano et al., 2017 The role of oligodendrocyte precursor cells expressing the GPR17 receptor in brain remodeling after stroke. Cell Death Dis 8: e2871.
  54. Bergdolt, S., A. Kovtun, Y. Hagele, A. Liedert, T. Schinke et al., 2017 Osteoblast-specific overexpression of complement receptor C5aR1 impairs fracture healing. PLoS One 12: e0179512.
  55. Asfar, P., F. Schortgen, J. Boisrame-Helms, J. Charpentier, E. Guerot et al., 2017 Hyperoxia and hypertonic saline in patients with septic shock (HYPERS2S): a two-by-two factorial, multicentre, randomised, clinical trial. Lancet Respir Med 5: 180-190.
  56. Wu, C. C., F. Kruse, M. D. Vasudevarao, J. P. Junker, D. C. Zebrowski et al., 2016 Spatially Resolved Genome-wide Transcriptional Profiling Identifies BMP Signaling as Essential Regulator of Zebrafish Cardiomyocyte Regeneration. Dev Cell 36: 36-49.
  57. Winkelmann VE, G. F., Hobi N, Dietl P, Frick M., 2016 Establishment of a co-culture to mimic the alveolar-capillary barrier in vitro, pp. S707. Acta Physiologica.
  58. Vigano, F., S. Schneider, M. Cimino, E. Bonfanti, P. Gelosa et al., 2016 GPR17 expressing NG2-Glia: Oligodendrocyte progenitors serving as a reserve pool after injury. Glia 64: 287-299.
  59. Stenzel, T., C. Weidgang, K. Wagner, F. Wagner, M. Groger et al., 2016 Association of Kidney Tissue Barrier Disrupture and Renal Dysfunction in Resuscitated Murine Septic Shock. Shock 46: 398-404.
  60. Sroka, R., J. Van Lint, S. F. Katz, M. R. Schneider, A. Kleger et al., 2016 Cortactin is a scaffolding platform for the E-cadherin adhesion complex and is regulated by protein kinase D1 phosphorylation. J Cell Sci 129: 2416-2429.
  61. Sinha, S., D. Hoshino, N. H. Hong, K. C. Kirkbride, N. E. Grega-Larson et al., 2016 Cortactin promotes exosome secretion by controlling branched actin dynamics. J Cell Biol 214: 197-213.
  62. Sehring, I. M., C. Jahn and G. Weidinger, 2016 Zebrafish fin and heart: what's special about regeneration? Curr Opin Genet Dev 40: 48-56.
  63. Schneider, S., A. Gruart, S. Grade, Y. Zhang, S. Kroger et al., 2016 Decrease in newly generated oligodendrocytes leads to motor dysfunctions and changed myelin structures that can be rescued by transplanted cells. Glia 64: 2201-2218.
  64. Schmidt, D., D. Peterlik, S. O. Reber, A. Lechner and D. N. Mannel, 2016 Induction of Suppressor Cells and Increased Tumor Growth following Chronic Psychosocial Stress in Male Mice. PLoS One 11: e0159059.
  65. Reber, S. O., P. H. Siebler, N. C. Donner, J. T. Morton, D. G. Smith et al., 2016 Immunization with a heat-killed preparation of the environmental bacterium Mycobacterium vaccae promotes stress resilience in mice. Proc Natl Acad Sci U S A 113: E3130-3139.
  66. Rapp, A. E., R. Bindl, S. Recknagel, A. Erbacher, I. Muller et al., 2016 Fracture Healing Is Delayed in Immunodeficient NOD/scidIL2Rgammacnull Mice. PLoS One 11: e0147465.
  67. Peter, S., M. M. Ten Brinke, J. Stedehouder, C. M. Reinelt, B. Wu et al., 2016 Dysfunctional cerebellar Purkinje cells contribute to autism-like behaviour in Shank2-deficient mice. Nat Commun 7: 12627.
  68. Masselink, W., N. J. Cole, F. Fenyes, S. Berger, C. Sonntag et al., 2016 A somitic contribution to the apical ectodermal ridge is essential for fin formation. Nature 535: 542-546.
  69. Liu, P., M. Baumgart, M. Groth, J. Wittmann, H. M. Jack et al., 2016 Dicer ablation in osteoblasts by Runx2 driven cre-loxP recombination affects bone integrity, but not glucocorticoid-induced suppression of bone formation. Sci Rep 6: 32112.
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  71. Kovtun, A., S. Bergdolt, R. Wiegner, P. Radermacher, M. Huber-Lang et al., 2016 The crucial role of neutrophil granulocytes in bone fracture healing. Eur Cell Mater 32: 152-162.
  72. Knoller, E., T. Stenzel, F. Broeskamp, R. Hornung, A. Scheuerle et al., 2016 Effects of Hyperoxia and Mild Therapeutic Hypothermia During Resuscitation From Porcine Hemorrhagic Shock. Crit Care Med 44: e264-277.
  73. Kalbitz, M., F. Fattahi, T. J. Herron, J. J. Grailer, L. Jajou et al., 2016 Complement Destabilizes Cardiomyocyte Function In Vivo after Polymicrobial Sepsis and In Vitro. J Immunol 197: 2353-2361.
  74. Kalbitz, M., F. Fattahi, J. J. Grailer, L. Jajou, E. A. Malan et al., 2016 Complement-induced activation of the cardiac NLRP3 inflammasome in sepsis. FASEB J 30: 3997-4006.
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  76. Huber-Lang, M., F. Gebhard, C. Q. Schmidt, A. Palmer, S. Denk et al., 2016 Complement therapeutic strategies in trauma, hemorrhagic shock and systemic inflammation - closing Pandora's box? Semin Immunol 28: 278-284.
  77. Heise, C., J. C. Schroeder, M. Schoen, S. Halbedl, D. Reim et al., 2016 Selective Localization of Shanks to VGLUT1-Positive Excitatory Synapses in the Mouse Hippocampus. Front Cell Neurosci 10: 106.
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  79. Harder, M. J., M. Anliker, B. Hochsmann, T. Simmet, M. Huber-Lang et al., 2016 Comparative Analysis of Novel Complement-Targeted Inhibitors, MiniFH, and the Natural Regulators Factor H and Factor H-like Protein 1 Reveal Functional Determinants of Complement Regulation. J Immunol 196: 866-876.
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