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Using experimental autoimmune encephalomyelitis as a model to study the effect of prenatal stress on fetal programming

Abstract Objectives: There is a growing evidence to suggest that the antecedents of some adult diseases can be traced back to their fetal origins. Despite extensive research on such diseases, to our knowledge, there has been no research investigating the relationship between the origins of multiple sclerosis (MS) disease and maternal infections. The aim of this study was to examine the role of prenatal exposure to endotoxin in fetal programming with respect to induction of susceptibility/vulnerability to MS. Methods: The pregnant dams were administered a single intraperitoneal injection of lipopolysaccharide in gestational day 10. The male offspring were weighed and examined for clinical signs of experimental autoimmune encephalomyelitis in a blinded fashion within 36 days after immunization (postnatal day 63–98). Results: Our data provide the evidence showing prenatal exposures to higher doses of Lipopolysaccharide resulted in an earlier onset of the disease, an augmentation of its clinical signs, and lower body weight in the prenatally Lipopolysaccharide -treated C57BL/6 mice after the immunization. Discussion: Therefore, the present research can provide evidence that prenatal stress may play a role in enhancing the clinical symptoms of experimental autoimmune encephalomyelitis/MS.