Divergent adaptive and innate immunological responses are observed in humans following blunt trauma.
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.
Kasten
Kevin R
KR
Division of Research, Department of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0558, USA.
Goetzman
Holly S
HS
Reid
Maria R
MR
Rasper
Alison M
AM
Adediran
Samuel G
SG
Robinson
Chad T
CT
Cave
Cindy M
CM
Solomkin
Joseph S
JS
Lentsch
Alex B
AB
Johannigman
Jay A
JA
Caldwell
Charles C
CC
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
D007371:Interferon-gamma; D051058:Oncogene Protein v-akt