Increased serum levels of macrophage migration inhibitory factor in autism spectrum disorders

These results identify high serum MIF levels are associated with severity of ASD. Further study is warranted on the precise involvement of MIF in ASD, and the mechanism by which MIF contributes to ASD pathogenesis.

One hundred and two Chinese children with ASD and same their age-sex matched typical development children were included. Concentrations of MIF were tested by Quantikine Human MIF Immunoassay. Serum levels of homocysteine (HCY), C-reactive protein (CRP) and serum Interleukin 6 (IL-6) were also tested. The influence of serum levels of MIF on ASD risk and ASD severity were performed by binary logistic regression analysis.

Macrophage migration inhibitory factor (MIF) has been suggested as a pivotal regulator of innate immunity and inflammatory. The aim of this study was to measure serum circulating levels of MIF in relation to the degree of the severity of autism spectrum disorders (ASD).

The serum levels of MIF in the children with ASD (24.7 ± 08.9 ng/ml) were significantly higher than those of control subjects (18.3 ± 5.5 ng/ml) (t = 6.134, P < 0.001). Levels of MIF increased with increasing severity of ASD as defined by the CARS score (P < 0.001). In multivariate model, MIF was associated with an increased risk of ASD (OR 1.11, 95% CI: 1.05-1.17; P < 0.001). MIF improved the combined model (HCY/CRP/IL-6) to predict ASD (P < 0.001). At admission, 68 children (66.7%) had a severe autism. In these children, the mean serum level of MIF was higher than in those children with mild to moderate autism (28.1 ± 8.5 ng/ml VS. 17.9 ± 4.7 ng/ml; t = 6.482, P < 0.001). In multivariate model, MIF was still associated with an increased risk of severe ASD (OR: 1.15, 95% CI: 1.04-1.19; P < 0.001). MIF improved the combined model (HCY/CRP/IL-6) to predict severe ASD (P < 0.001). Conclusions: These results identify high serum MIF levels are associated with severity of ASD. Further study is warranted on the precise involvement of MIF in ASD, and the mechanism by which MIF contributes to ASD pathogenesis.