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. Huber-Lang, M., J.D. Lambris, and P.A. Ward. 2018. Innate immune responses to trauma. Nat Immunol. 19:327-341.
  2. Böbel, T.S., S.B. Hackl, D. Langgartner, M.N. Jarczok, N. Rohleder, G.A. Rook, C.A. Lowry, H. Gundel, C. Waller, and S.O. Reber. 2018. Less immune activation following social stress in rural vs. urban participants raised with regular or no animal contact, respectively. Proc Natl Acad Sci U S A. 115:5259-5264.
  3. Wiesner, D., L. Tar, B. Linkus, A. Chandrasekar, F. Olde Heuvel, L. Dupuis, W. Tsao, P.C. Wong, A. Ludolph, and F. Roselli. 2018. Reversible induction of TDP-43 granules in cortical neurons after traumatic injury. Exp Neurol. 299:15-25.
  4. Werner, J.U., K. Todter, P. Xu, L. Lockhart, M. Jahnert, P. Gottmann, A. Schurmann, L. Scheja, M. Wabitsch, and U. Knippschild. 2018. Comparison of Fatty Acid and Gene Profiles in Skeletal Muscle in Normal and Obese C57BL/6J Mice before and after Blunt Muscle Injury. Frontiers in physiology. 9:19.
  5. Tu, J., S. Stoner, P.D. Fromm, T. Wang, D. Chen, J. Tuckermann, M.S. Cooper, M.J. Seibel, and H. Zhou. 2018. Endogenous glucocorticoid signaling in chondrocytes attenuates joint inflammation and damage. FASEB J. 32:478-487.
  6. Rapp, A.E., Y. Hachemi, J. Kemmler, M. Koenen, J. Tuckermann, and A. Ignatius. 2018. Induced global deletion of glucocorticoid receptor impairs fracture healing. FASEB J. 32:2235-2245.
  7. Prystaz, K., K. Kaiser, A. Kovtun, M. Haffner-Luntzer, V. Fischer, A.E. Rapp, A. Liedert, G. Strauss, G.H. Waetzig, S. Rose-John, and A. Ignatius. 2018. Distinct effects of interleukin-6 classic and trans-signaling in bone fracture healing. The American Journal of Pathology. 188:474-490.
  8. Mettang, M., S.N. Reichel, M. Lattke, A. Palmer, A. Abaei, V. Rasche, M. Huber-Lang, B. Baumann, and T. Wirth. 2018. IKK2/NF-kappaB signaling protects neurons after traumatic brain injury. FASEB J. 32:1916-1932.
  9. Martin, T., A. Moglich, I. Felix, C. Fortsch, A. Rittlinger, A. Palmer, S. Denk, J. Schneider, L. Notbohm, M. Vogel, H. Geiger, S. Paschke, M. Huber-Lang, and H. Barth. 2018. Rho-inhibiting C2IN-C3 fusion toxin inhibits chemotactic recruitment of human monocytes ex vivo and in mice in vivo. Arch Toxicol. 92:323-336.
  10. Lee, S., P. Liu, R. Teinturier, J. Jakob, M. Tschaffon, A. Tasdogan, R. Wittig, S. Hoeller, D. Baumhoer, L. Frappart, S. Vettorazzi, P. Bertolino, C. Zhang, and J. Tuckermann. 2018. Deletion of Menin in craniofacial osteogenic cells in mice elicits development of mandibular ossifying fibroma. Oncogene. 37:616-626.
  11. Haffner-Luntzer, M., A. Kovtun, I. Lackner, Y. Modinger, S. Hacker, A. Liedert, J. Tuckermann, and A. Ignatius. 2018. Estrogen receptor alpha- (ERalpha), but not ERbeta-signaling, is crucially involved in mechanostimulation of bone fracture healing by whole-body vibration. Bone. 110:11-20.
  12. Hachemi, Y., A. Rapp, A.K. Picke, G. Weidinger, A. Ignatius, and J. Tuckermann. 2018. Molecular Mechanisms of Glucocorticoids on Skeleton and Regeneration after Fracture. J Mol Endocrinol.
  13. Denk, S., S. Weckbach, P. Eisele, C.K. Braun, R. Wiegner, J.J. Ohmann, L. Wrba, F.M. Hoenes, P. Kellermann, P. Radermacher, U. Wachter, S. Hafner, O. McCook, A. Schultze, A. Palmer, S. Braumuller, F. Gebhard, and M. Huber-Lang. 2018. Role of Hemorrhagic Shock in Experimental Polytrauma. Shock. 49:154-163.
  14. Amann, E.M., M.T. Rojewski, S. Rodi, D. Fürst, J. Fiedler, A. Palmer, S. Braumüller, M. Huber-Lang, H. Schrezenmeier, and R.E. Brenner. 2018. Systemic recovery and therapeutic effects of transplanted allogenic and xenogenic mesenchymal stromal cells in a rat blunt chest trauma model. In Cytotherapy. Vol. 20. 218-231.
  15. Zimprich, A., G. Mroz, C. Meyer Zu Reckendorf, S. Anastasiadou, P. Forstner, L. Garrett, S.M. Holter, L. Becker, J. Rozman, C. Prehn, B. Rathkolb, K. Moreth, W. Wurst, T. Klopstock, M. Klingenspor, J. Adamski, E. Wolf, R. Bekeredjian, H. Fuchs, V. Gailus-Durner, M.H. de Angelis, and B. Knöll. 2017. Serum Response Factor (SRF) Ablation Interferes with Acute Stress-Associated Immediate and Long-Term Coping Mechanisms. Mol Neurobiol. 54:8242-8262.
  16. 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.
  17. Wehner, D., T.M. Tsarouchas, A. Michael, C. Haase, G. Weidinger, M.M. Reimer, T. Becker, and C.G. Becker. 2017. Wnt signaling controls pro-regenerative Collagen XII in functional spinal cord regeneration in zebrafish. Nat Commun. 8:126.
  18. Wanner, R., M. Gey, A. Abaei, D. Warnecke, L. de Roy, L. Dürselen, V. Rasche, and B. Knöll. 2017. Functional and Molecular Characterization of a Novel Traumatic Peripheral Nerve-Muscle Injury Model. Neuromolecular Med. 19:357-374.
  19. Sportelli, M.C., E. Tutuncu, R.A. Picca, M. Valentini, A. Valentini, C. Kranz, B. Mizaikoff, H. Barth, and N. Cioffi. 2017. Inhibiting P. fluorescens biofilms with fluoropolymer-embedded silver nanoparticles: an in-situ spectroscopic study. Sci Rep. 7:11870.
  20. Singh, K., L. Krug, A. Basu, P. Meyer, N. Treiber, S. Vander Beken, M. Wlaschek, S. Kochanek, W. Bloch, H. Geiger, P. Maity, and K. Scharffetter-Kochanek. 2017. Alpha-Ketoglutarate Curbs Differentiation and Induces Cell Death in Mesenchymal Stromal Precursors with Mitochondrial Dysfunction. Stem Cells. 35:1704-1718.
  21. Seichter, F., J. Vogt, P. Radermacher, and B. Mizaikoff. 2017. Nonlinear calibration transfer based on hierarchical Bayesian models and Lagrange Multipliers: Error bounds of estimates via Monte Carlo - Markov Chain sampling. Anal Chim Acta. 951:32-45.
  22. Seichter, F., J. Vogt, P. Radermacher, and B. Mizaikoff. 2017. Response-surface fits and calibration transfer for the correction of the oxygen effect in the quantification of carbon dioxide via FTIR spectroscopy. Anal Chim Acta. 972:16-27.
  23. Schimunek, L., R. Serve, M.P.J. Teuben, P. Stormann, B. Auner, M. Woschek, R. Pfeifer, K. Horst, T.P. Simon, M. Kalbitz, R. Sturm, H.C. Pape, F. Hildebrand, I. Marzi, and B. Relja. 2017. Early decreased TLR2 expression on monocytes is associated with their reduced phagocytic activity and impaired maturation in a porcine polytrauma model. PloS one. 12:e0187404.
  24. Radermacher, P., S.M. Maggiore, and A. Mercat. 2017. Fifty Years of Research in ARDS. Gas Exchange in Acute Respiratory Distress Syndrome. Am J Respir Crit Care Med. 196:964-984.
  25. Pfaender, S., A.K. Sauer, S. Hagmeyer, K. Mangus, L. Linta, S. Liebau, J. Bockmann, G. Huguet, T. Bourgeron, T.M. Boeckers, and A.M. Grabrucker. 2017. Zinc deficiency and low enterocyte zinc transporter expression in human patients with autism related mutations in SHANK3. Sci Rep. 7:45190.
  26. Owlarn, S., F. Klenner, D. Schmidt, F. Rabert, A. Tomasso, H. Reuter, M.A. Mulaw, S. Moritz, L. Gentile, G. Weidinger, and K. Bartscherer. 2017. Generic wound signals initiate regeneration in missing-tissue contexts. Nat Commun. 8:2282.
  27. Nussbaum, B.L., T. Stenzel, T. Merz, A. Scheuerle, O. McCook, U. Wachter, J.A. Vogt, J. Matallo, H. Gassler, M. Groger, M. Matejovic, E. Calzia, L. Lampl, M. Georgieff, P. Moller, P. Asfar, P. Radermacher, and S. Hafner. 2017. Hyperoxia or Therapeutic Hypothermia During Resuscitation from Non-Lethal Hemorrhagic Shock in Swine. Shock. 48:564-570.
  28. Ng, D.Y.W., R. Vill, Y. Wu, K. Koynov, Y. Tokura, W. Liu, S. Sihler, A. Kreyes, S. Ritz, H. Barth, U. Ziener, and T. Weil. 2017. Directing intracellular supramolecular assembly with N-heteroaromatic quaterthiophene analogues. Nat Commun. 8:1850.
  29. Mueller, K.M., K. Hartmann, D. Kaltenecker, S. Vettorazzi, M. Bauer, L. Mauser, S. Amann, S. Jall, K. Fischer, H. Esterbauer, T.D. Muller, M.H. Tschop, C. Magnes, J. Haybaeck, T. Scherer, N. Bordag, J.P. Tuckermann, and R. Moriggl. 2017. Adipocyte Glucocorticoid Receptor Deficiency Attenuates Aging- and HFD-Induced Obesity and Impairs the Feeding-Fasting Transition. Diabetes. 66:272-286.
  30. Merz, T., J.A. Vogt, U. Wachter, E. Calzia, C. Szabo, R. Wang, P. Radermacher, and O. McCook. 2017. Impact of hyperglycemia on cystathionine-gamma-lyase expression during resuscitated murine septic shock. Intensive Care Med Exp. 5:30.
  31. Merz, T., T. Stenzel, B. Nussbaum, M. Wepler, C. Szabo, R. Wang, P. Radermacher, and O. McCook. 2017. Cardiovascular disease and resuscitated septic shock lead to the downregulation of the H2S-producing enzyme cystathionine-gamma-lyase in the porcine coronary artery. Intensive Care Med Exp. 5:17.
  32. Magadum, A., Y. Ding, L. He, T. Kim, M.D. Vasudevarao, Q. Long, K. Yang, N. Wickramasinghe, H.V. Renikunta, N. Dubois, G. Weidinger, Q. Yang, and F.B. Engel. 2017. Live cell screening platform identifies PPARdelta as a regulator of cardiomyocyte proliferation and cardiac repair. Cell Res. 27:1002-1019.
  33. Losing, P., C.E. Niturad, M. Harrer, C.M.Z. Reckendorf, T. Schatz, D. Sinske, H. Lerche, S. Maljevic, and B. Knöll. 2017. SRF modulates seizure occurrence, activity induced gene transcription and hippocampal circuit reorganization in the mouse pilocarpine epilepsy model. Mol Brain. 10:30.
  34. Liu, P., S. Lee, J. Knöll, A. Rauch, S. Ostermay, J. Luther, N. Malkusch, U.H. Lerner, M.M. Zaiss, M. Neven, R. Wittig, M. Rauner, J.P. David, P. Bertolino, C.X. Zhang, and J.P. Tuckermann. 2017. Loss of menin in osteoblast lineage affects osteocyte-osteoclast crosstalk causing osteoporosis. Cell Death Differ. 24:672-682.
  35. Lattke, M., S.N. Reichel, A. Magnutzki, A. Abaei, V. Rasche, P. Walther, D.P. Calado, B. Ferger, T. Wirth, and B. Baumann. 2017. Transient IKK2 activation in astrocytes initiates selective non-cell-autonomous neurodegeneration. Mol Neurodegener. 12:16.
  36. Langgartner, D., D. Peterlik, S. Foertsch, A.M. Fuchsl, P. Brokmann, P.J. Flor, Z. Shen, J.G. Fox, N. Uschold-Schmidt, C.A. Lowry, and S.O. Reber. 2017. Individual differences in stress vulnerability: The role of gut pathobionts in stress-induced colitis. Brain Behav Immun. 64:23-32.
  37. Kroner, J., A. Kovtun, J. Kemmler, J.J. Messmann, G. Strauss, S. Seitz, T. Schinke, M. Amling, J. Kotrba, J. Dudeck, A. Dudeck, and A. Ignatius. 2017. Mast cells are critical regulators of bone fracture-induced inflammation and osteoclast formation and activity. J Bone Miner Res. 32:2431–2444.
  38. Kreidler, A.M., R. Benz, and H. Barth. 2017. Chloroquine derivatives block the translocation pores and inhibit cellular entry of Clostridium botulinum C2 toxin and Bacillus anthracis lethal toxin. Arch Toxicol. 91:1431-1445.
  39. Kovtun, A., S. Bergdolt, Y. Hagele, R. Matthes, J.D. Lambris, M. Huber-Lang, and A. Ignatius. 2017. Complement receptors C5aR1 and C5aR2 act differentially during the early immune response after bone fracture but are similarly involved in bone repair. Sci Rep. 7:14061.
  40. Kalbitz, M., C. Waller, M. Huber-Lang, F. Gebhard, C. Thiemermann, and P. Radermacher. 2017. Oxygen in the Heart: How Much is too Much? Shock. 47:531-532.
  41. Kalbitz, M., S. Schwarz, B. Weber, B. Bosch, J. Pressmar, F.M. Hoenes, C.K. Braun, K. Horst, T.P. Simon, R. Pfeifer, P. Stormann, H. Hummler, F. Gebhard, H.C. Pape, M. Huber-Lang, F. Hildebrand, and T.R. Group. 2017. Cardiac Depression in Pigs after Multiple Trauma - Characterization of Posttraumatic Structural and Functional Alterations. Sci Rep. 7:17861.
  42. Kalbitz, M., J. Pressmar, J. Stecher, B. Weber, M. Weiss, S. Schwarz, E. Miltner, F. Gebhard, and M. Huber-Lang. 2017. The Role of Troponin in Blunt Cardiac Injury After Multiple Trauma in Humans. World J Surg. 41:162-169.
  43. Kalbitz, M., E.M. Amann, B. Bosch, A. Palmer, A. Schultze, J. Pressmar, B. Weber, M. Wepler, F. Gebhard, H. Schrezenmeier, R. Brenner, and M. Huber-Lang. 2017. Experimental blunt chest trauma-induced myocardial inflammation and alteration of gap-junction protein connexin 43. PloS one. 12:e0187270.
  44. Itkin, T., A. Kumari, E. Schneider, S. Gur-Cohen, C. Ludwig, R. Brooks, O. Kollet, K. Golan, E. Khatib-Massalha, C.M. Russo, J.D. Chisholm, A. Rouhi, H. Geiger, E. Hornstein, W.G. Kerr, F. Kuchenbauer, and T. Lapidot. 2017. MicroRNA-155 promotes G-CSF-induced mobilization of murine hematopoietic stem and progenitor cells via propagation of CXCL12 signaling. Leukemia. 31:1247-1250.
  45. Husecken, Y., S. Muche, M. Kustermann, M. Klingspor, A. Palmer, S. Braumuller, M. Huber-Lang, K.M. Debatin, and G. Strauss. 2017. MDSCs are induced after experimental blunt chest trauma and subsequently alter antigen-specific T cell responses. Sci Rep. 7:12808.
  46. Huber-Lang, M., K.N. Ekdahl, R. Wiegner, K. Fromell, and B. Nilsson. 2017. Auxiliary activation of the complement system and its importance for the pathophysiology of clinical conditions. Semin Immunopathol.
  47. Hartmann, C., P. Radermacher, M. Wepler, and B. Nubaum. 2017. Non-Hemodynamic Effects of Catecholamines. Shock.
  48. Hartmann, C., B. Nussbaum, E. Calzia, P. Radermacher, and M. Wepler. 2017. Gaseous Mediators and Mitochondrial Function: The Future of Pharmacologically Induced Suspended Animation? Frontiers in physiology. 8:691.
  49. Hartmann, C., M. Loconte, E. Antonucci, M. Holzhauser, T. Holle, D. Katzsch, T. Merz, O. McCook, U. Wachter, J.A. Vogt, A. Hoffmann, M. Wepler, M. Groger, M. Matejovic, E. Calzia, M. Georgieff, P. Asfar, P. Radermacher, and B.L. Nussbaum. 2017. Effects of Hyperoxia During Resuscitation From Hemorrhagic Shock in Swine With Preexisting Coronary Artery Disease. Crit Care Med. 45:e1270-e1279.
  50. Hartmann, C., S. Hafner, A. Scheuerle, P. Moller, M. Huber-Lang, B. Jung, B. Nubaum, O. McCook, M. Groger, F. Wagner, S. Weber, B. Stahl, E. Calzia, M. Georgieff, C. Szabo, R. Wang, P. Radermacher, and K. Wagner. 2017. The Role of Cystathionine-gamma-Lyase In Blunt Chest Trauma in Cigarette Smoke Exposed Mice. Shock. 47:491-499.
  51. Halbgebauer, R., C.K. Braun, S. Denk, B. Mayer, P. Cinelli, P. Radermacher, G.A. Wanner, H.P. Simmen, F. Gebhard, D. Rittirsch, and M. Huber-Lang. 2017. Hemorrhagic shock drives glycocalyx, barrier and organ dysfunction early after polytrauma. J Crit Care. 44:229-237.
  52. Hagemeyer, N., K.M. Hanft, M.A. Akriditou, N. Unger, E.S. Park, E.R. Stanley, O. Staszewski, L. Dimou, and M. Prinz. 2017. Microglia contribute to normal myelinogenesis and to oligodendrocyte progenitor maintenance during adulthood. Acta Neuropathol. 134:441-458.
  53. Hafner, S., K. Wagner, S. Weber, M. Groger, M. Wepler, O. McCook, A. Scheuerle, B. Stahl, M. Huber-Lang, B. Jung, E. Calzia, M. Georgieff, P. Moller, M. Frick, P. Radermacher, and F. Wagner. 2017. Role of the Purinergic Receptor P2XR4 After Blunt Chest Trauma in Cigarette Smoke-Exposed Mice. Shock. 47:193-199.
  54. Haffner-Luntzer, M., F. Muller-Graf, R. Matthys, Y. Hägele, V. Fischer, R. Jonas, A. Abaei, F. Gebhard, V. Rasche, and A. Ignatius. 2017. Evaluation of high-resolution In Vivo MRI for longitudinal analysis of endochondral fracture healing in mice. PloS one. 12:e0174283.
  55. Haffner-Luntzer, M., F. Müller-Graf, R. Matthys, A. Abaei, R. Jonas, F. Gebhard, V. Rasche, and A. Ignatius. 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.
  56. 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. European Journal of Medical Research. 33:23.
  57. Guidi, N., M. Sacma, L. Standker, K. Soller, G. Marka, K. Eiwen, J.M. Weiss, F. Kirchhoff, T. Weil, J.A. Cancelas, M.C. Florian, and H. Geiger. 2017. Osteopontin attenuates aging-associated phenotypes of hematopoietic stem cells. EMBO J. 36:1463.
  58. Galuppo, P., S. Vettorazzi, J. Hovelmann, C.J. Scholz, J.P. Tuckermann, J. Bauersachs, and D. Fraccarollo. 2017. The glucocorticoid receptor in monocyte-derived macrophages is critical for cardiac infarct repair and remodeling. FASEB J. 31:5122-5132.
  59. Gačanin, J., A. Kovtun, S. Fischer, V. Schwager, J. Quambusch, S.L. Kuan, W. Liu, F. Boldt, C. Li, Z. Yang, D. Liu, Y. Wu, T. Weil, H. Barth, and A. Ignatius. 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.
  60. Foertsch, S., M. Haffner-Luntzer, J. Kroner, F. Gross, K. Kaiser, M. Erber, S.O. Reber, and A. Ignatius. 2017. Chronic psychosocial stress disturbs long-bone growth in adolescent mice. Dis Model Mech. 10:1399-1409.
  61. Foertsch, S., A.M. Fuchsl, S.D. Faller, H. Holzer, D. Langgartner, J. Messmann, G. Strauss, and S.O. Reber. 2017. Splenic glucocorticoid resistance following psychosocial stress requires physical injury. Sci Rep. 7:15730.
  62. Fattahi, F., M. Kalbitz, E.A. Malan, E. Abe, L. Jajou, M.S. Huber-Lang, M. Bosmann, M.W. Russell, F.S. Zetoune, and P.A. Ward. 2017. Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction. FASEB J. 31:4129-4139.
  63. Ernst, K., J. Schmid, M. Beck, M. Hagele, M. Hohwieler, P. Hauff, A.K. Uckert, A. Anastasia, M. Fauler, T. Jank, K. Aktories, M.R. Popoff, C. Schiene-Fischer, A. Kleger, M. Muller, M. Frick, and H. Barth. 2017. Hsp70 facilitates trans-membrane transport of bacterial ADP-ribosylating toxins into the cytosol of mammalian cells. Sci Rep. 7:2724.
  64. Denk, S., R.P. Taylor, R. Wiegner, E.M. Cook, M.A. Lindorfer, K. Pfeiffer, S. Paschke, T. Eiseler, M. Weiss, E. Barth, J.D. Lambris, M. Kalbitz, T. Martin, H. Barth, D.A.C. Messerer, F. Gebhard, and M.S. Huber-Lang. 2017. Complement C5a-Induced Changes in Neutrophil Morphology During Inflammation. Scand J Immunol. 86:143-155.
  65. Denk, S., M.D. Neher, D.A.C. Messerer, R. Wiegner, B. Nilsson, D. Rittirsch, K. Nilsson-Ekdahl, S. Weckbach, A. Ignatius, M. Kalbitz, F. Gebhard, M.E. Weiss, J. Vogt, P. Radermacher, J. Kohl, J.D. Lambris, and M.S. Huber-Lang. 2017. Complement C5a Functions as a Master Switch for the pH Balance in Neutrophils Exerting Fundamental Immunometabolic Effects. J Immunol. 198:4846-4854.
  66. Chandrasekar, A., F.O. Heuvel, A. Palmer, B. Linkus, A.C. Ludolph, T.M. Boeckers, B. Relja, M. Huber-Lang, and F. Roselli. 2017. Acute ethanol administration results in a protective cytokine and neuroinflammatory profile in traumatic brain injury. Int Immunopharmacol. 51:66-75.
  67. Braun, C.K., M. Kalbitz, R. Halbgebauer, P. Eisele, D.A.C. Messerer, S. Weckbach, A. Schultze, S. Braumuller, F. Gebhard, and M.S. Huber-Lang. 2017. Early structural changes of the heart after experimental polytrauma and hemorrhagic shock. PloS one. 12:e0187327.
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