482 Traumatic Brain Injury and Hemorrhage in a Juvenile Rat Model of Polytrauma Leads to Immunosuppression and Splenic Alterations. (1st April 2022)

• Record Type: Journal Article
• Authors: Sribnick, Eric A.; Warner, Timothy; Hall, Mark
• Is Part Of: Neurosurgery. Volume 68(2022)Supplement 1
• Page Start: 119
• Page End: 119
• Publication Date: 2022-04-01
• Subjects: Nervous system -- Surgery -- Periodicals; 617.48005
• DOI: 10.1227/NEU.0000000000001880_482
• Languages: English
• ISSNs: 0148-396X

Abstract

Abstract : INTRODUCTION: Traumatic brain injury (TBI) is a common cause of morbidity and mortality for which there are no pharmacotherapeutic agents. We have previously shown, with clinical data and in an animal model, that TBI with a concurrent extra-cranial injury can reliably lead to post-injury immunosuppression. METHODS: To assess the clinical relevance of our combined model, we examined lungs for evidence of spontaneous bacterial colonization. Prepubescent (28 day old) rats were injured with a moderately severe controlled cortical impact model and then had 25% blood volume removed by arteriotomy. Blood and spleen samples at post-injury day 1 were incubated with T or B cell immunostimulant and were examined for IFN-G production using an Eli-Spot assay. Spleen samples were examined at this timepoint for apoptosis using Annexin V staining. Lungs were also harvested and plated on blood agar to examine spontaneous bacterial colonization. RESULTS: Stimulation of whole blood samples and spleen with PMA at post-injury day 1 were associated with significant decreases in IFN-G-positive cells/million, as compared with samples from sham animals. As compared to sham, spleen samples from injured animals showed a marked increase in splenocyte apoptosis in the white pulp of the spleen. Lung samples, plated on blood agar, showed a 300% increase in colonies per plate in injured animals. CONCLUSION: These data add to a growing body of literature suggesting that severe trauma can lead to immunosuppression. Our findings further suggest a potential role for the spleen in altering leukocyte function following injury.