| First Author | Vandermosten L | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Issue | 1 | Pages | 13835 |
| PubMed ID | 29062028 | Mgi Jnum | J:255556 |
| Mgi Id | MGI:6109397 | Doi | 10.1038/s41598-017-14288-x |
| Citation | Vandermosten L, et al. (2017) 11beta-hydroxysteroid dehydrogenase type 1 has no effect on survival during experimental malaria but affects parasitemia in a parasite strain-specific manner. Sci Rep 7(1):13835 |
| abstractText | 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, 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD1) converts intrinsically inert GCs into active GCs. 11beta-HSD1 shapes endogenous GC action and is immunomodulatory. We investigated the role of 11beta-HSD1 in two mouse models of malaria. 11beta-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, 11beta-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 11beta-HSD1 deficiency though plasma levels of IL-4, IL-6 and TNF-alpha were slightly affected by 11beta-HSD1 deficiency, dependent on the infecting parasite. These data suggest that 11beta-HSD1 is not crucial for survival of experimental malaria, but alters its progression in a parasite strain-specific manner. |
