Plasma Anti-Glial Fibrillary Acidic Protein Autoantibody Levels during the Acute and Chronic Phases of Traumatic Brain Injury: A Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot Study

Kevin K.W. Wang, Zhihui Yang, John K. Yue, Zhiqun Zhang, Ethan A. Winkler, Ava M. Puccio, Ramon Diaz-Arrastia, Hester F. Lingsma, Esther L. Yuh, Pratik Mukherjee, Alex B. Valadka, Wayne A. Gordon, David O. Okonkwo, Geoffrey T. Manley, Shelly R. Cooper, Kristen Dams-O'Connor, Allison J. Hricik, Tomoo Inoue, Andrew I.R. Maas, David K. MenonDavid M. Schnyer, Tuhin K. Sinha, Mary J. Vassar

Research output: Contribution to journalArticlepeer-review

47 Scopus citations

Abstract

We described recently a subacute serum autoantibody response toward glial fibrillary acidic protein (GFAP) and its breakdown products 5-10 days after severe traumatic brain injury (TBI). Here, we expanded our anti-GFAP autoantibody (AutoAb[GFAP]) investigation to the multicenter observational study Transforming Research and Clinical Knowledge in TBI Pilot (TRACK-TBI Pilot) to cover the full spectrum of TBI (Glasgow Coma Scale 3-15) by using acute (<24 h) plasma samples from 196 patients with acute TBI admitted to three Level I trauma centers, and a second cohort of 21 participants with chronic TBI admitted to inpatient TBI rehabilitation. We find that acute patients self-reporting previous TBI with loss of consciousness (LOC) (n = 43) had higher day 1 AutoAb[GFAP] (mean ± standard error: 9.11 ± 1.42; n = 43) than healthy controls (2.90 ± 0.92; n = 16; p = 0.032) and acute patients reporting no previous TBI (2.97 ± 0.37; n = 106; p < 0.001), but not acute patients reporting previous TBI without LOC (8.01 ± 1.80; n = 47; p = 0.906). These data suggest that while exposure to TBI may trigger the AutoAb[GFAP] response, circulating antibodies are elevated specifically in acute TBI patients with a history of TBI. AutoAb[GFAP] levels for participants with chronic TBI (average post-TBI time 176 days or 6.21 months) were also significantly higher (15.08 ± 2.82; n = 21) than healthy controls (p < 0.001). These data suggest a persistent upregulation of the autoimmune response to specific brain antigen(s) in the subacute to chronic phase after TBI, as well as after repeated TBI insults. Hence, AutoAb[GFAP] may be a sensitive assay to study the dynamic interactions between post-injury brain and patient-specific autoimmune responses across acute and chronic settings after TBI.

Original languageEnglish (US)
Pages (from-to)1270-1277
Number of pages8
JournalJournal of neurotrauma
Volume33
Issue number13
DOIs
StatePublished - Jul 1 2016
Externally publishedYes

Keywords

  • autoantibody
  • autoimmunity
  • biomarkers
  • glia
  • traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology

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