ArticleScientific reports2017
11β-hydroxysteroid dehydrogenase type 1 has no effect on survival during experimental malaria but affects parasitemia in a parasite strain-specific manner.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Larval Ascariasis Triggers Unresolved Anemia, Persistent Inflammation, and Chronic Pulmonary Disease after Single and Reinfection in a Dose-Dependent Manner in Mice.ACS infectious diseases · 2025Article
- Deletion of Hsd11b1 suppresses caloric restriction-induced bone marrow adiposity in male but not female mice.The Journal of endocrinology · 2024Article
- Alveolar macrophages and monocyte subpopulations duringHeliyon · 2024Article
- Adrenal hormones mediate disease tolerance in malaria.Nature communications · 2018Article
- Experimental malaria-associated acute respiratory distress syndrome is dependent on the parasite-host combination and coincides with normocyte invasion.Malaria journal · 2018Article
- 11β-hydroxysteroid dehydrogenase-1 deficiency alters brain energy metabolism in acute systemic inflammation.Brain, behavior, and immunity · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
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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Registered trials
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