Modulatory role of vitamin A on the Candida albicans-induced immune response in human monocytes
Klassert, Tilman E.
Heyl, Kerstin A.
Mansour, Michael M.
MetadataShow full item record
CitationKlassert, Tilman E., Anja Hanisch, Julia Bräuer, Esther Klaile, Kerstin A. Heyl, Michael M. Mansour, Jenny M. Tam, Jatin M. Vyas, and Hortense Slevogt. 2014. “Modulatory role of vitamin A on the Candida albicans-induced immune response in human monocytes.” Medical Microbiology and Immunology 203 (6): 415-424. doi:10.1007/s00430-014-0351-4. http://dx.doi.org/10.1007/s00430-014-0351-4.
AbstractBeyond its well-documented role in reproduction, embryogenesis and maintenance of body tissues, vitamin A has attracted considerable attention due to its immunomodulatory effects on both the innate and the adaptive immune responses. In infectious diseases, vitamin A has been shown to have a host-protective effect in infections of bacterial, viral or protozoan origin. Nevertheless, its impact in fungal infections remains unknown. Meanwhile, the frequency of invasive mycoses keeps on growing, with Candida albicans being the major opportunistic fungal pathogen and associated with high mortality. In the present work, we explored the impact of all-trans retinoic acid (atRA), the most active metabolite of vitamin A, on the innate immune response against C.albicans in human monocytes. Our results show a strong immunomodulatory role for atRA, leading to a significant down-regulation of the fungi-induced expression and secretion of the pro-inflammatory cytokines TNFα, IL6 and IL12. Moreover, atRA significantly suppressed the expression of Dectin-1, a major fungal pattern recognition receptor, as well as the Dectin-1-dependent cytokine production. Both RAR-dependent and RAR-independent mechanisms seem to play a role in the atRA-mediated immunomodulation. Our findings open a new direction to elucidate the role of vitamin A on the immune function during fungal infections. Electronic supplementary material The online version of this article (doi:10.1007/s00430-014-0351-4) contains supplementary material, which is available to authorized users.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:13454767
- HMS Scholarly Articles 
Contact administrator regarding this item (to report mistakes or request changes)