Severe Traumatic Head Injury Affects Systemic Cytokine Expression

Overview

Journal J Am Coll Surg

Specialties General Surgery
Gynecology & Obstetrics

Date 2012 Feb 21

PMID 22342787

Citations 9

Authors

Damien J LaPar

Laura H Rosenberger

Dustin M Walters

Traci L Hedrick

Brian R Swenson

Jeffrey S Young

Lesly A Dossett

Addison K May

Robert G Sawyer

Affiliations

Soon will be listed here.

Abstract

Background: The neuroimmunologic effect of traumatic head injury remains ill-defined. This study aimed to characterize systemic cytokine profiles among traumatically injured patients to assess the effect of traumatic head injury on the systemic inflammatory response.

Study Design: For 5 years, 1,022 patients were evaluated from a multi-institutional Trauma Immunomodulatory Database. Patients were stratified by presence of severe head injury (SHI; head Injury Severity Score ≥4, n = 335) vs nonsevere head injury (NHI; head Injury Severity Score ≤3, n = 687). Systemic cytokine expression was quantified by ELISA within 72 hours of admission. Patient factors, outcomes, and cytokine profiles were compared by univariate analyses.

Results: SHI patients were more severely injured with higher mortality, despite similar ICU infection and ventilator-associated pneumonia rates. Expression of early proinflammatory cytokines, interleukin-6 (p < 0.001) and tumor necrosis factor-α (p = 0.02), was higher among NHI patients, and expression of immunomodulatory cytokines, interferon-γ (p = 0.01) and interleukin-12 (p = 0.003), was higher in SHI patients. High tumor necrosis factor-α levels in NHI patients were associated with mortality (p = 0.01), increased mechanical ventilation (p = 0.02), and development of ventilator-associated pneumonia (p = 0.01). Alternatively, among SHI patients, high interleukin-2 levels were associated with survival, decreased mechanical ventilation, and absence of ventilator-associated pneumonia.

Conclusions: The presence of severe traumatic head injury significantly alters systemic cytokine expression and exerts an immunomodulatory effect. Early recognition of these profiles can allow for targeted intervention to reduce patient morbidity and mortality.

Citing Articles

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Using IL-6 concentrations in the first 24 h following trauma to predict immunological complications and mortality in trauma patients: a meta-analysis.

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References

Csuka E, Morganti-Kossmann M, Lenzlinger P, Joller H, Trentz O, Kossmann T . IL-10 levels in cerebrospinal fluid and serum of patients with severe traumatic brain injury: relationship to IL-6, TNF-alpha, TGF-beta1 and blood-brain barrier function. J Neuroimmunol. 1999; 101(2):211-21. DOI: 10.1016/s0165-5728(99)00148-4. View

Baker S, ONeill B, HADDON Jr W, Long W . The injury severity score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma. 1974; 14(3):187-96. View

Hama T, Miyamoto M, Tsukui H, Nishio C, Hatanaka H . Interleukin-6 as a neurotrophic factor for promoting the survival of cultured basal forebrain cholinergic neurons from postnatal rats. Neurosci Lett. 1989; 104(3):340-4. DOI: 10.1016/0304-3940(89)90600-9. View

Correale J, Villa A . The neuroprotective role of inflammation in nervous system injuries. J Neurol. 2004; 251(11):1304-16. DOI: 10.1007/s00415-004-0649-z. View

Taupin V, Toulmond S, Serrano A, Benavides J, Zavala F . Increase in IL-6, IL-1 and TNF levels in rat brain following traumatic lesion. Influence of pre- and post-traumatic treatment with Ro5 4864, a peripheral-type (p site) benzodiazepine ligand. J Neuroimmunol. 1993; 42(2):177-85. DOI: 10.1016/0165-5728(93)90008-m. View

Kossmann T, Hans V, Imhof H, Stocker R, Grob P, Trentz O . Intrathecal and serum interleukin-6 and the acute-phase response in patients with severe traumatic brain injuries. Shock. 1995; 4(5):311-7. DOI: 10.1097/00024382-199511000-00001. View

Sanderson K, Raghupathi R, Saatman K, Martin D, Miller G, McIntosh T . Interleukin-1 receptor antagonist attenuates regional neuronal cell death and cognitive dysfunction after experimental brain injury. J Cereb Blood Flow Metab. 1999; 19(10):1118-25. DOI: 10.1097/00004647-199910000-00008. View

Ziebell J, Morganti-Kossmann M . Involvement of pro- and anti-inflammatory cytokines and chemokines in the pathophysiology of traumatic brain injury. Neurotherapeutics. 2010; 7(1):22-30. PMC: 5084109. DOI: 10.1016/j.nurt.2009.10.016. View

Kossmann T, Hans V, Imhof H, Trentz O, Morganti-Kossmann M . Interleukin-6 released in human cerebrospinal fluid following traumatic brain injury may trigger nerve growth factor production in astrocytes. Brain Res. 1996; 713(1-2):143-52. DOI: 10.1016/0006-8993(95)01501-9. View

10.

Ott L, McClain C, Gillespie M, Young B . Cytokines and metabolic dysfunction after severe head injury. J Neurotrauma. 1994; 11(5):447-72. DOI: 10.1089/neu.1994.11.447. View

11.

Boddie D, Currie D, Eremin O, Heys S . Immune suppression and isolated severe head injury: a significant clinical problem. Br J Neurosurg. 2003; 17(5):405-17. DOI: 10.1080/02688690310001611198. View

12.

Morganti-Kossmann M, Satgunaseelan L, Bye N, Kossmann T . Modulation of immune response by head injury. Injury. 2007; 38(12):1392-400. DOI: 10.1016/j.injury.2007.10.005. View

13.

Goodman J, Robertson C, Grossman R, Narayan R . Elevation of tumor necrosis factor in head injury. J Neuroimmunol. 1990; 30(2-3):213-7. DOI: 10.1016/0165-5728(90)90105-v. View

14.

Kadhim H, Duchateau J, Sebire G . Cytokines and brain injury: invited review. J Intensive Care Med. 2008; 23(4):236-49. DOI: 10.1177/0885066608318458. View

15.

Jones N, Prior M, Burden-Teh E, Marsden C, Morris P, Murphy S . Antagonism of the interleukin-1 receptor following traumatic brain injury in the mouse reduces the number of nitric oxide synthase-2-positive cells and improves anatomical and functional outcomes. Eur J Neurosci. 2005; 22(1):72-8. DOI: 10.1111/j.1460-9568.2005.04221.x. View

16.

Helmy A, De Simoni M, Guilfoyle M, Carpenter K, Hutchinson P . Cytokines and innate inflammation in the pathogenesis of human traumatic brain injury. Prog Neurobiol. 2011; 95(3):352-72. DOI: 10.1016/j.pneurobio.2011.09.003. View

17.

Bone R, Grodzin C, Balk R . Sepsis: a new hypothesis for pathogenesis of the disease process. Chest. 1997; 112(1):235-43. DOI: 10.1378/chest.112.1.235. View

18.

Lenzlinger P, Morganti-Kossmann M, Laurer H, McIntosh T . The duality of the inflammatory response to traumatic brain injury. Mol Neurobiol. 2002; 24(1-3):169-81. DOI: 10.1385/MN:24:1-3:169. View

19.

Bone R . The pathogenesis of sepsis. Ann Intern Med. 1991; 115(6):457-69. DOI: 10.7326/0003-4819-115-6-457. View

20.

Ghajar J . Traumatic brain injury. Lancet. 2000; 356(9233):923-9. DOI: 10.1016/S0140-6736(00)02689-1. View