Over-expression of TGF-β1 gene in medication free Schizophrenia

Background and purpose: Immunological pathways play a crucial role in developing and precipitating neuropsychiatric disorders. Although the exact pathogenesis of schizophrenia is unknown, the possible role of genetic and biomarker involvement of the immune system is gaining attention. Here we quantified the mRNA expression of cytokines as a key role player of the immune system from the peripheral blood mononuclear cells of patients with schizophrenia and healthy controls to identify the differentially expressed genes. Methods: Sixteen medication-free schizophrenia patients and 16 healthy subjects were enrolled in the current study. To investigate the desired expression level of mRNAs including TGP-beta 1, IL-1 beta, IL-23, TNF-alpha, NF-kappa B, and BDNF, quantitative real-time PCR was performed using specific oligonucleotide primers and the Applied Bin systems StepOne (TM) real time PCR system. DNA methylation was also analyzed through methylation-specific polymerase chain reaction (MSP). Results: TGF beta 1 was significantly up-regulated in peripheral blood mononuclear cells of patients vs. healthy individuals (P value = 0.03). In addition, we found a significant correlation between the positive symptom scale and TGF-beta 1 gene overexpression (r = 0.536, P = 0.039). However, we did not observe any statistically significant differences for the methylation status of CpG Islands 1 and 2 between the patients and normal group. No statistical significance was found either for gene expression of IL-1 beta,8 (P = 0.32), IL-23 (P = 0.12), TNF-alpha (P = 0.87), NF-kappa B (P = 0.07), and BDNF (P = 0.33). Conclusions: Although the number of medication-free schizophrenia patients is extremely limited, our data highlighted the potential role of TGF-beta 1 as a regulatory cytokine in complex inflammatory mechanism involved in medication-free schizophrenia. In addition, we observed that increased level of TGF-beta 1 mRNA in this disease might not be under methylation as an epigenetic control element at the genomic level.