Pregnancy an
d birth complications, particularly those associate
d with maternal inflammation an
d fetal hypoxia, are associate
d with increase
d risk for schizophrenia later in life. However, the molecular mechanisms un
derlying these associations are not fully
delineate
d. This stu
dy sought to examine the effect of exposure to maternal inflammation on risk of
developing psychosis in a
dulthoo
d. Maternal serum levels of pro-inflammatory Th1 cytokines (IL-2, interferon gamma [IFN-γ], IL-12) an
d Th17 cytokines (IL-1b, IL-6, IL-8, tumor necrosis factor alpha [TNF-α], granulocyte macrophage colony stimulating factor [gm-csf]) an
d anti-inflammatory Th2 cytokines (IL-4, IL-5, an
d IL-13) an
d Treg cytokines (IL-10) were evaluate
d for association with later psychosis in the offspring.
d="absSec_2">Methods
d="sp0040">Subjects were 43 adults with psychoses and 43 matched controls followed from gestation as part of the Philadelphia cohort of the National Collaborative Perinatal Project. Adult symptoms of psychosis were assessed via medical records review and confirmed with a validation study. Archived maternal serum samples collected at the time of birth were analyzed for cytokine levels using a multiplex bead assay.
d="absSec_3">Results
d="sp0045">Individuals exposed to elevated maternal levels of anti-inflammatory Th2 cytokines (≥ 75th percentile) were significantly less likely to develop psychosis in adulthood.
d="absSec_4">Conclusions
d="sp0050">These results may suggest that increased maternal levels of anti-inflammatory cytokines during the perinatal period could protect against the development of psychosis.