ABSTRACT
Background: a potential role of toxoplasmosis for immune dysfunction has been suggested in Autism spectrum disorder [ASD]. The imbalances in pro- and anti-inflammatory processes could markedly hinder. host defense mechanisms important for immune control of the Toxoplasmosis. To test this hypothesis, we investigated evidence of differential cytokines release in plasma samples obtained from 3 to 10 year-old children with ASD compared with age-matched typically developing [TD] children with toxoplasmosis and without toxoplasmosis
Methodology: twenty four [18 boys and 6 girls] autistic children were included in this study. Their age ranged from 3- 10 years old [mean = 69.25 +/- 25.6 month]. There were diagnosed according to DSM 1V criteria. Control group included eighteen non-autistic children. The control group was divided in to two groups 1] control with toxoplasmosis [9 children]. 2] Control without toxoplasmosis [9 children]. All were subjected to uull history, clinical examination, and estimation of serum Toxoplasma IgG, serum TNF- alpha, INF -gamma and catalaze enzyme
Results: sex autistic children were Toxoplasma IgG positive [25%]]. Level of catalase enzyme was significantly lower in all patient than the control [P =0.048] with no significant differences of TNF- alpha and INF-gamma [P = 0.272, = 0.137] respectively. Serum TNF- alpha -level in autistic children with toxoplasmosis was highly significantly correlated with severity of autistic criteria assessed by Childhood Autistic Rating Scale [CARS] [r = 0.986, P=.0.000]. There was no significant correlation of INF-gamma and catalase level with severity of autistic criteria [r= 0.312, P= 0.5] [r= 0.720, P= 0.189]. INF-gamma and catalase levels were significantly correlated with severity of autism [r= - 0.496, P= 0.036] and [r= 0.650, P= 0.004] its autistic children without toxoplasmosis. TNF level was not significantly correlated with total CARS [r =000, P=l] in the same group
Conclusion: toxoplasmosis may result in immune modulation among ASD patients. These fluctuations in cytokines could result in a recurrent profuse multiplication of Toxoplasma gonadi in the brain associated with persistent neuroinflammation