| Abstract | Schistosomiasismansoniisawidespreadparasiticinfectionthatmayleadtoseveralseriouscomplications,suchas
hepaticperiportalfibrosisandportalhypertension,mainlyduetodepositionofschistosomeeggsinthetissues.
However,peopleinendemicareasinfrequentlyexhibitseverepathologyandcomplications;thismaybeexplained,in
part, bymodulationofthediseaseinindigenouspopulationsby in utero exposuretotheparasite.Thisstudy
investigatedthedifferencesbetweenmicebornto Schistosomamansoni-infectedmothersandthoseborntonon-
infectedonesinsubsequentpostnatalschistosomalinfections.Wefoundthattheintensityofinfection,evidencedby
hepaticeggload,wasmuchreducedinmiceborntoinfectedmothers.Nodifferencewasfoundasregardstotaland
Schistosoma-specificimmunoglobulinlevelsexceptfortotalIgG.Thelevelsofgeneexpressionoftworegulatory
cytokines,namelyinterleukin-12(IL-12)andtransforminggrowthfactorbeta(TGF-b) werefoundtobesignificantly
increasedinprenatallyexposedanimals.Moreover,liverfibrosiswassignificantlydecreasedinanimalsborntoinfected
mothersasrevealedbyhistopathologicalandhistochemicalexaminationaswellasbyimmunohistochemical
identificationofactivatedhepaticstellatecells(HSCs)usingantibodyagainstglialfibrillaryacidicprotein(GFAP).
In conclusion,congenitalexposureto S. mansoni seems toamelioratetheimmunopathologicalchangesinfuture
postnatalinfections. |