The future of murine sepsis and trauma research models

Recent comparisons of the murine and human transcriptome in health and disease have called into question the appropriateness of the use of murine models for human sepsis and trauma research. More specifically, researchers have debated the suitability of mouse models of severe inflammation that is intended for eventual translation to human patients. This mini‐review outlines this recent research, as well as specifically defines the arguments for and against murine models of sepsis and trauma research based on these transcriptional studies. In addition, we review newer advancements in murine models of infection and injury and define what we envision as an evolving but viable future for murine studies of sepsis and trauma.

[1]  A. Mohr,et al.  Chronic restraint stress after injury and shock is associated with persistent anemia despite prolonged elevation in erythropoietin levels , 2015, The journal of trauma and acute care surgery.

[2]  D. Livingston,et al.  Can mesenchymal stem cells reverse chronic stress-induced impairment of lung healing following traumatic injury? , 2015, The journal of trauma and acute care surgery.

[3]  H. Baker,et al.  Advanced age is associated with worsened outcomes and a unique genomic response in severely injured patients with hemorrhagic shock , 2015, Critical Care.

[4]  M. Singer,et al.  Detailed Characterization of a Long-Term Rodent Model of Critical Illness and Recovery , 2015, Critical care medicine.

[5]  F. Collins,et al.  A new initiative on precision medicine. , 2015, The New England journal of medicine.

[6]  Shane J. Neph,et al.  A comparative encyclopedia of DNA elements in the mouse genome , 2014, Nature.

[7]  Keizo Takao,et al.  Genomic responses in mouse models greatly mimic human inflammatory diseases , 2014, Proceedings of the National Academy of Sciences.

[8]  L. Moldawer,et al.  A Better Understanding of Why Murine Models of Trauma Do Not Recapitulate the Human Syndrome* , 2014, Critical care medicine.

[9]  Heinz Redl,et al.  Abandon the Mouse Research Ship? Not Just Yet! , 2014, Shock.

[10]  Francis S Collins,et al.  Policy: NIH to balance sex in cell and animal studies , 2014, Nature.

[11]  Saeid Amini-Nik,et al.  Animal models in burn research , 2014, Cellular and Molecular Life Sciences.

[12]  H. Baker,et al.  Protective Immunity and Defects in the Neonatal and Elderly Immune Response to Sepsis , 2014, The Journal of Immunology.

[13]  H. Baker,et al.  Aged Mice Are Unable To Mount an Effective Myeloid Response to Sepsis , 2014, The Journal of Immunology.

[14]  H. Baker,et al.  Persistent inflammation, immunosuppression, and catabolism syndrome after severe blunt trauma , 2014, The journal of trauma and acute care surgery.

[15]  T. Higgins,et al.  Sepsis and Scientific Revolutions , 2013, Critical care medicine.

[16]  Brandon M. Welch,et al.  The Need for Clinical Decision Support Integrated with the Electronic Health Record for the Clinical Application of Whole Genome Sequencing Information , 2013, Journal of Personalized Medicine.

[17]  H. Perlman,et al.  Traumatic brain injury–induced alterations in peripheral immunity , 2013, The journal of trauma and acute care surgery.

[18]  Marc S. Williams,et al.  Integration of Genomics into the Electronic Health Record: Mapping Terra Incognita , 2013, Genetics in Medicine.

[19]  Christopher G. Chute,et al.  Some experiences and opportunities for big data in translational research , 2013, Genetics in Medicine.

[20]  M. Fink.  Animal models of sepsis , 2013, Virulence.

[21]  R. Tompkins,et al.  Reply to Osterburg et al.: To study human inflammatory diseases in humans , 2013, Proceedings of the National Academy of Sciences.

[22]  H. Perlman,et al.  Humanizing the mouse: in defense of murine models of critical illness. , 2013, American journal of respiratory and critical care medicine.

[23]  H. Baker,et al.  Identification and Description of a Novel Murine Model for Polytrauma and Shock , 2013, Critical care medicine.

[24]  R. Hotchkiss,et al.  Immunosuppression in sepsis: a novel understanding of the disorder and a new therapeutic approach. , 2013, The Lancet. Infectious diseases.

[25]  T. Miyakawa,et al.  Genomic responses in mouse models poorly mimic human inflammatory diseases , 2013 .

[26]  R. Gamelli,et al.  Genomic responses in mouse models poorly mimic human inflammatory diseases , 2013, Proceedings of the National Academy of Sciences.

[27]  D. Koller,et al.  Conservation and divergence in the transcriptional programs of the human and mouse immune systems , 2013, Proceedings of the National Academy of Sciences.

[28]  M. Delano,et al.  The Acute Immunological Response to Blood Transfusion Is Influenced by Polymicrobial Sepsis , 2012, Shock.

[29]  Elizabeth R. Duffy,et al.  Sepsis Chronically in MARS: Systemic Cytokine Responses Are Always Mixed Regardless of the Outcome, Magnitude, or Phase of Sepsis , 2012, The Journal of Immunology.

[30]  R. Hotchkiss,et al.  Interleukin-7 ameliorates immune dysfunction and improves survival in a 2-hit model of fungal sepsis. , 2012, The Journal of infectious diseases.

[31]  L. Moldawer,et al.  Persistent inflammation and immunosuppression: A common syndrome and new horizon for surgical intensive care , 2012, The journal of trauma and acute care surgery.

[32]  D. Schoenfeld,et al.  Benchmarking Outcomes in the Critically Injured Trauma Patient and the Effect of Implementing Standard Operating Procedures , 2012, Annals of surgery.

[33]  D. Heffernan,et al.  Mechanisms of Indirect Acute Lung Injury: A Novel Role for the Coinhibitory Receptor, Programmed Death-1 , 2012, Annals of surgery.

[34]  John D. Storey,et al.  A genomic storm in critically injured humans , 2011, The Journal of experimental medicine.

[35]  Steven S. Henley,et al.  Early blood product and crystalloid volume resuscitation: risk association with multiple organ dysfunction after severe blunt traumatic injury. , 2011, The Journal of trauma.

[36]  Y. Vodovotz,et al.  Models of lower extremity damage in mice: time course of organ damage and immune response. , 2011, The Journal of surgical research.

[37]  R. Lefering,et al.  Epidemiology and risk factors of sepsis after multiple trauma: An analysis of 29,829 patients from the Trauma Registry of the German Society for Trauma Surgery* , 2011, Critical care medicine.

[38]  L. Kao,et al.  The epidemiology of sepsis in general surgery patients. , 2011, The Journal of trauma.

[39]  H. Saito,et al.  The effects of aging on pulmonary oxidative damage, protein nitration, and extracellular superoxide dismutase down-regulation during systemic inflammation. , 2011, Free radical biology & medicine.

[40]  Jyotika Sharma,et al.  Attenuated Response of Aged Mice to Respiratory Francisella novicida Is Characterized by Reduced Cell Death and Absence of Subsequent Hypercytokinemia , 2010, PloS one.

[41]  L. Moldawer,et al.  Cecal Ligation and Puncture , 2010, Current protocols in immunology.

[42]  Ira J. Kalet,et al.  Feasibility of incorporating genomic knowledge into electronic medical records for pharmacogenomic clinical decision support , 2010, BMC Bioinformatics.

[43]  Stephen L. Jones,et al.  Sepsis in general surgery: the 2005-2007 national surgical quality improvement program perspective. , 2010, Archives of surgery.

[44]  D. Rittirsch,et al.  EARLY EXPRESSION CHANGES OF COMPLEMENT REGULATORY PROTEINS AND C5a RECEPTOR (CD88) ON LEUKOCYTES AFTER MULTIPLE INJURY IN HUMANS , 2010, Shock.

[45]  C. Coopersmith,et al.  Characterization and Modulation of the Immunosuppressive Phase of Sepsis , 2010, Infection and Immunity.

[46]  C. Probst,et al.  Late death after multiple severe trauma: when does it occur and what are the causes? , 2009, The Journal of trauma.

[47]  C. Coopersmith,et al.  Effects of aging on the immunopathologic response to sepsis , 2009, Critical care medicine.

[48]  T. Fabian,et al.  Improved survival of critically ill trauma patients treated with recombinant human erythropoietin. , 2008, The Journal of trauma.

[49]  G. Su,et al.  Attenuating burn wound inflammation improves pulmonary function and survival in a burn-pneumonia model , 2007, Critical care medicine.

[50]  L. Moldawer,et al.  MyD88-dependent expansion of an immature GR-1+CD11b+ population induces T cell suppression and Th2 polarization in sepsis , 2007, The Journal of experimental medicine.

[51]  J. Sunderram,et al.  Rapid increase in hospitalization and mortality rates for severe sepsis in the United States: A trend analysis from 1993 to 2003* , 2007, Critical care medicine.

[52]  R. Hotchkiss,et al.  PNEUMONIA AFTER CECAL LIGATION AND PUNCTURE: A CLINICALLY RELEVANT "TWO-HIT" MODEL OF SEPSIS , 2006, Shock.

[53]  J. Siddiqui,et al.  Mechanisms of Mortality in Early and Late Sepsis , 2006, Infection and Immunity.

[54]  Scott M Sasser,et al.  Preventing death and disability through the timely provision of prehospital trauma care. , 2006, Bulletin of the World Health Organization.

[55]  C. Hughes,et al.  Of Mice and Not Men: Differences between Mouse and Human Immunology , 2004, The Journal of Immunology.

[56]  A. Baue.  Sepsis, systemic inflammatory response syndrome, multiple organ dysfunction syndrome, and multiple organ failure: are trauma surgeons lumpers or splitters? , 2003, The Journal of trauma.

[57]  C. Coopersmith,et al.  Effects of Age on Mortality and Antibiotic Efficacy in Cecal Ligation and Puncture , 2003, Shock.

[58]  D. Remick,et al.  ANTIBIOTIC TREATMENT INFLUENCES OUTCOME IN MURINE SEPSIS: MEDIATORS OF INCREASED MORBIDITY , 1998, Shock.

[59]  S. Garg,et al.  Exogenous interleukin-10 fails to decrease the mortality or morbidity of sepsis. , 1998, Critical care medicine.

[60]  D. Bates,et al.  Epidemiology of sepsis syndrome in 8 academic medical centers. , 1997, JAMA.

[61]  A. Baue.  Multiple organ failure, multiple organ dysfunction syndrome, and systemic inflammatory response syndrome. Why no magic bullets? , 1997, Archives of surgery.

[62]  N. Goldstein.  Mice are not men! , 1994, Hawaii medical journal.

[63]  J. Maessen,et al.  Tumour Necrosis Factor Alpha (TNF‐α) and Interleukin 6 in a Zymosan‐Induced Shock Model , 1990 .

[64]  Kun Huang,et al.  Injury, Large-Scale Collaborative Research Program , 2015 .

[65]  P. Giannoudis,et al.  30 years of polytrauma care: An analysis of the change in strategies and results of 4849 cases treated at a single institution. , 2009, Injury.

[66]  J. Maessen,et al.  Tumour necrosis factor alpha (TNF-alpha) and interleukin 6 in a zymosan-induced shock model. , 1990, Scandinavian journal of immunology.

[67]  I. Chaudry,et al.  Hemorrhage without tissue trauma produces immunosuppression and enhances susceptibility to sepsis. , 1987, Archives of surgery.