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In order to determine if such a perinatal insult affects the course of demyelination in adulthood as \u201csecond hit,\u201d we simulated perinatal bacterial inflammation by systemic administration of lipopolysaccharide (LPS) to either pregnant mice or newborn animals. Demyelination was later induced in adult animals by cuprizone [<jats:italic>bis<\/jats:italic>(cyclohexylidenehydrazide)], which causes oligodendrocyte death with subsequent demyelination accompanied by strong microgliosis and astrogliosis. A single LPS injection at embryonic day 13.5 did not have an impact on demyelination in adulthood. In contrast, serial postnatal LPS injections (P0\u2010P8) caused an early delay of myelin removal in the corpus callosum, which was paralleled by reduced numbers of activated microglia. During remyelination, postnatal LPS treatment enhanced early remyelination with a concomitant increase of mature oligodendrocytes. Furthermore, the postnatal LPS challenge impacts the phenotype of microglia since an elevated mRNA expression of microglia related genes such as TREM 2, CD11b, TNF\u2010\u03b1, TGF\u2010\u03b21, HGF, FGF\u20102, and IGF\u20101 was found in these preconditioned mice during early demyelination. These data demonstrate that postnatal inflammation has long\u2010lasting effects on microglia functions and modifies the course of demyelination and remyelination in adulthood. 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