TY - JOUR
AR - CEI-2020-1-105
TI - Evaluation of Immunologic Function of Peripheral Blood Monocytes from Schizophrenic Patients in Response to Toxoplasma Gondii
AU - Ahmad Ali Noorbala, 
AU - Ahmad Zavaran Hosseini, 
AU - Esfandiar Azizi, 
AU - Saiyad, Bastaminejad
AU - Sara Soudi, 
JO - Clinical and Experimental Investigations
PY - 2020
DA - Wed 12, Feb 2020
SN - 2674-5054
DO - http://dx.doi.org/10.31487/j.CEI.2020.01.05
UR - https://www.sciencerepository.org/evaluation-of-immunologic-function_CEI-2020-1-105 
KW - Schizophrenia, T. gondii, monocyte, miR-155, miR-146a
AB - Background: It has been suggested that the function of myeloid immune cells, especially macrophages in
schizophrenia patients (SCZ), is impaired. Considering the role of macrophages in induction of
inflammatory responses, the purpose of this study is to examine the response of monocyte-derived
macrophages (MDM) of schizophrenia patients to Toxoplasma gondii (T. gondii) challenge.
Materials and Methods: MDMs were generated from 20 SCZ and 10 healthy controls (HC). The cells
were exposed to T. gondii. The Cytokine (IL-10, IL-12, IL-6, and TNF-α) and nitric oxide (NO) productions
were measured. The expression of miR146a and miR155 was examined using qPCR.
Results: The level of NO was significantly higher in the supernatant of MDMs of SCZ compared with the
HC (P≤0.05) in response to T. gondii. There was no difference in cytokine (IL-10, IL-12, IL-6, and TNF-α)
production of SCZ compared to the controls. The effect of miR-155/ miR-146a on inflammatory cytokine
production was confirmed using anti-miRNAs. There were no significant effect in miR-155/ miR-146a
expression of macrophages of schizophrenia patients to T. gondii compared to control.
Conclusion: In this study, although the cytokine response and the amount of miR-155/ miR-146a expression
of macrophages to T. gondii was not significantly different between the schizophrenia patients and the
healthy subjects, the significant differences in the production of nitric oxide strengthen the hypothesis of
the functional failure of these cells.