title: Divergent adaptive and innate immunological responses are observed in humans following blunt trauma.
abstract: BACKGROUND
  The immune response to trauma has traditionally been modeled to consist of the systemic inflammatory response syndrome (SIRS) followed by the compensatory anti-inflammatory response syndrome (CARS). We investigated these responses in a homogenous cohort of male, severe blunt trauma patients admitted to a University Hospital surgical intensive care unit (SICU). After obtaining consent, peripheral blood was drawn up to 96 hours following injury. The enumeration and functionality of both myeloid and lymphocyte cell populations were determined.
  
  
  RESULTS
  Neutrophil numbers were observed to be elevated in trauma patients as compared to healthy controls. Further, neutrophils isolated from trauma patients had increased raft formation and phospho-Akt. Consistent with this, the neutrophils had increased oxidative burst compared to healthy controls. In direct contrast, blood from trauma patients contained decreased naïve T cell numbers. Upon activation with a T cell specific mitogen, trauma patient T cells produced less IFN-gamma as compared to those from healthy controls. Consistent with these results, upon activation, trauma patient T cells were observed to have decreased T cell receptor mediated signaling.
  
  
  CONCLUSIONS
  These results suggest that following trauma, there are concurrent and divergent immunological responses. These consist of a hyper-inflammatory response by the innate arm of the immune system concurrent with a hypo-inflammatory response by the adaptive arm.
authors.affiliation: Division of Research, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0558, USA.
authors.forename: Kevin R
authors.initials: KR
authors.lastname: Kasten
authors.forename: Holly S
authors.initials: HS
authors.lastname: Goetzman
authors.forename: Maria R
authors.initials: MR
authors.lastname: Reid
authors.forename: Alison M
authors.initials: AM
authors.lastname: Rasper
authors.forename: Samuel G
authors.initials: SG
authors.lastname: Adediran
authors.forename: Chad T
authors.initials: CT
authors.lastname: Robinson
authors.forename: Cindy M
authors.initials: CM
authors.lastname: Cave
authors.forename: Joseph S
authors.initials: JS
authors.lastname: Solomkin
authors.forename: Alex B
authors.initials: AB
authors.lastname: Lentsch
authors.forename: Jay A
authors.initials: JA
authors.lastname: Johannigman
authors.forename: Charles C
authors.initials: CC
authors.lastname: Caldwell
mesh_terms: D056704:Adaptive Immunity; D000328:Adult; D006801:Humans; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000235:genetics; D008231:Lymphopenia; D008297:Male; D021962:Membrane Microdomains / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D051058:Oncogene Protein v-akt / Q000276:immunology / Q000378:metabolism; D010085:Oxidative Phosphorylation; D016897:Respiratory Burst; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D014947:Wounds and Injuries / Q000097:blood
chemical_list: D007371:Interferon-gamma; D051058:Oncogene Protein v-akt