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Impaired CD8 T cell response to viral infection following acute spinal cord injury
Journal article   Peer reviewed

Impaired CD8 T cell response to viral infection following acute spinal cord injury

Diana Maria Norden, John R Bethea and Jiu Jiang
The Journal of immunology (1950), v 198(1_Supplement), pp 78-78.7
01 May 2017

Abstract

Abstract Trauma to the spinal cord disrupts essential communication between the central nervous system and the immune system. This is highly important as patients with spinal cord injury (SCI) are at greater risk for infections that increase morbidity and mortality. Previous studies have confirmed immune depression in mouse models of chronic SCI. In mice, injury at the high thoracic level disrupts sympathetic output and leads to sustained elevations of norepinephrine in the spleen. SCI patients, however, are at high risk for infections acutely after SCI while hospitalized. Here, we induced a mid thoracic injury where integrity of the sympathetic response is maintained and investigated the antiviral response to influenza an acute timepoint. Mice received a 70kdyn contusion injury at T9 and were challenged intranasally with influenza virus (HKx31, H3N2) 7 days after injury. Following infection, injured mice had a diminished CD8 T cell response with decreased numbers of virus-specific CD8 cells in the lungs. Effector functions were also impaired in injured mice. Expansion of CD62Llow/CD44high effector CD8 T cells was reduced in injured mice and recruitment of CD8 T cells to the lungs was decreased compared to uninjured mice. In addition, the number of intracellular IFNγ-secreting CD8 T cells after in vitro stimulation with virus-specific peptide was reduced in both spleen and lung of injured mice. Overall, these data show an impaired CD8 T cell response to viral infection after acute SCI and suggest that immune depression following SCI occurs rapidly and may be independent of chronic norepinephrine elevations.

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