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Malaria is a global disease associated with considerable mortality and morbidity. An appropriately balanced immune response is crucial in determining the outcome of malarial infection. The glucocorticoid (GC) metabolising enzyme, 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1) converts intrinsically inert GCs into active GCs. 11β-HSD1 shapes endogenous GC action and is immunomodulatory. We investigated the role of 11β-HSD1 in two mouse models of malaria. 11β-HSD1 deficiency did not affect survival after malaria infection, but it increased disease severity and parasitemia in mice infected with  Plasmodium chabaudi  AS. In contrast, 11β-HSD1 deficiency rather decreased parasitemia in mice infected with the reticulocyte-restricted parasite  Plasmodium berghei  NK65 1556Cl1. Malaria-induced antibody production and pathology were unaltered by 11β-HSD1 deficiency though plasma levels of IL-4, IL-6 and TNF-α were slightly affected by 11β-HSD1 deficiency, dependent on the infecting parasite. These data suggest that 11β-HSD1 is not crucial for survival of experimental malaria, but alters its progression in a parasite strain-specific manner.

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11β-hydroxysteroid dehydrogenase type 1 has no effect on survival during experimental malaria but affects parasitemia in a parasite strain-specific manner