Previous work has demonstrated that the hormone prolactin promotes oligodendrocyte precursor proliferation and\nremyelination following lysolecithin-induced demyelination of the mouse spinal cord. Prolactin, however, can elicit\npro-inflammatory responses, and its use in the prototypical demyelinating and inflammatory condition, multiple\nsclerosis (MS), should thus be approached cautiously. Here, we sought to determine whether recombinant prolactin\ncould alter the course of experimental autoimmune encephalomyelitis (EAE), an inflammatory animal model of MS.\nConsistent with previous literature, we found that prolactin activated leukocytes in vitro. Daily treatment with prolactin\nfrom around the time of onset of clinical signs, for 9 (days 9 to 17) or 25 (days 9 to 33) days did not increase clinical or\nhistological signs of EAE over that of vehicle-treated mice. Instead, the combination of prolactin and a suboptimal dose\nof recombinant murine interferon-? resulted in (days 9 to 17 group) or trended towards (days 9 to 33 group), a greater\namelioration of clinical signs of EAE, compared to either treatment alone or to vehicle controls. Histological analyses\ncorroborated the clinical EAE data. These results suggest that prolactin may be beneficial when administered in\ncombination with interferon-? in MS.
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