Shared immune and repair markers during experimental toxoplasma chronic brain infection and schizophrenia
Schizophrenia Bulletin , Volume 42 - Issue 2 p. 386- 395
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.
|Animal model, Biomarker, Toxoplasma gondii|
|This work was funded by the European Commission 7th Framework Programme; grant id fp7/286334 - Advanced Immuno-neuro-endocrine Diagnostics in Psychiatry (PSYCH-AID)|
|Organisation||Department of Neuroscience|
Tomasik, J.J, Schultz, T.L, Kluge, W, Yolken, R.H, Bahn, S, & Carruthers, V.B. (2016). Shared immune and repair markers during experimental toxoplasma chronic brain infection and schizophrenia. Schizophrenia Bulletin, 42(2), 386–395. doi:10.1093/schbul/sbv134