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Galectin-3 impacts Cryptococcus neoformans infection through direct antifungal effects.
- Source :
-
Nature communications [Nat Commun] 2017 Dec 06; Vol. 8 (1), pp. 1968. Date of Electronic Publication: 2017 Dec 06. - Publication Year :
- 2017
-
Abstract
- Cryptococcus neoformans is an encapsulated fungal pathogen that causes cryptococcosis, which is a major opportunistic infection in immunosuppressed individuals. Mammalian β-galactoside-binding protein Galectin-3 (Gal-3) modulates the host innate and adaptive immunity, and plays significant roles during microbial infections including some fungal diseases. Here we show that this protein plays a role also in C. neoformans infection. We find augmented Gal-3 serum levels in human and experimental infections, as well as in spleen, lung, and brain tissues of infected mice. Gal-3-deficient mice are more susceptible to cryptococcosis than WT animals, as demonstrated by the higher fungal burden and lower animal survival. In vitro experiments show that Gal-3 inhibits fungal growth and exerts a direct lytic effect on C. neoformans extracellular vesicles (EVs). Our results indicate a direct role for Gal-3 in antifungal immunity whereby this molecule affects the outcome of C. neoformans infection by inhibiting fungal growth and reducing EV stability, which in turn could benefit the host.
- Subjects :
- Adaptive Immunity
Animals
Bacterial Capsules drug effects
Blood Proteins
Brain immunology
Cryptococcosis microbiology
Cryptococcus neoformans growth & development
Cryptococcus neoformans immunology
Cytokines metabolism
Disease Models, Animal
Galectin 3 blood
Galectin 3 genetics
Galectins
Gene Expression
Humans
Lung immunology
Macrophages drug effects
Male
Mice
Mice, Inbred C57BL
Spleen immunology
Antifungal Agents immunology
Antifungal Agents pharmacology
Cryptococcosis drug therapy
Cryptococcosis immunology
Cryptococcus neoformans drug effects
Galectin 3 immunology
Galectin 3 pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 2041-1723
- Volume :
- 8
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Nature communications
- Publication Type :
- Academic Journal
- Accession number :
- 29213074
- Full Text :
- https://doi.org/10.1038/s41467-017-02126-7