Shared immune and repair markers during experimental toxoplasma chronic brain infection and schizophrenia

Jakub Tomasik, Tracey L. Schultz, Wolfgang Kluge, Robert H. Yolken, Sabine Bahn, Vern B. Carruthers

Research output: Contribution to journalArticlepeer-review

Abstract

Chronic neurologic infection with Toxoplasma gondii is relatively common in humans and is one of the strongest known risk factors for schizophrenia. Nevertheless, the exact neuropathological mechanisms linking T gondii infection and schizophrenia remain unclear. Here we utilize a mouse model of chronic T gondii infection to identify protein biomarkers that are altered in serum and brain samples at 2 time points during chronic infection. Furthermore, we compare the identified biomarkers to those differing between "postmortem" brain samples from 35 schizophrenia patients and 33 healthy controls. Our findings suggest that T gondii infection causes substantial and widespread immune activation indicative of neural damage and reactive tissue repair in the animal model that partly overlaps with changes observed in the brains of schizophrenia patients. The overlapping changes include increases in C-reactive protein (CRP), interleukin-1 beta (IL-1β), interferon gamma (IFNγ), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular cell adhesion molecule 1 (VCAM-1). Potential roles of these factors in the pathogenesis of schizophrenia and toxoplasmosis are discussed. Identifying a defined set of markers shared within the pathophysiological landscape of these diseases could be a key step towards understanding their specific contributions to pathogenesis.

Original languageEnglish (US)
Pages (from-to)386-395
Number of pages10
JournalSchizophrenia bulletin
Volume42
Issue number2
DOIs
StatePublished - Mar 2016

Keywords

  • Animal model
  • Biomarker
  • Toxoplasma gondii

ASJC Scopus subject areas

  • Psychiatry and Mental health

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