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- Title
Cell wall N-glycan of Candida albicans ameliorates early hyper- and late hypo-immunoreactivity in sepsis.
- Authors
Kawakita, Masataka; Oyama, Taiki; Shirai, Ikuma; Tanaka, Shuto; Akaki, Kotaro; Abe, Shinya; Asahi, Takuma; Cui, Guangwei; Itoh, Fumie; Sasaki, Masato; Shibata, Nobuyuki; Ikuta, Koichi; Hatakeyama, Tomomitsu; Takahara, Kazuhiko
- Abstract
Severe infection often causes a septic cytokine storm followed by immune exhaustion/paralysis. Not surprisingly, many pathogens are equipped with various anti-inflammatory mechanisms. Such mechanisms might be leveraged clinically to control septic cytokine storms. Here we show that N-glycan from pathogenic C. albicans ameliorates mouse sepsis through immunosuppressive cytokine IL-10. In a sepsis model using lipopolysaccharide (LPS), injection of the N-glycan upregulated serum IL-10, and suppressed pro-inflammatory IL-1β, TNF-α and IFN-γ. The N-glycan also improved the survival of mice challenged by LPS. Analyses of structurally defined N-glycans from several yeast strains revealed that the mannose core is key to the upregulation of IL-10. Knocking out the C-type lectin Dectin-2 abrogated the N-glycan-mediated IL-10 augmentation. Furthermore, C. albicans N-glycan ameliorated immune exhaustion/immune paralysis after acute inflammation. Our results suggest a strategy where the immunosuppressive mechanism of one pathogen can be applied to attenuate a severe inflammation/cytokine storm caused by another pathogen. Kawakita et al use a murine sepsis model to show that N-glycan from pathogenic C. albicans ameliorates sepsis - and thus improves survival - through upregulation of the cytokine IL-10. This study demonstrates a potential strategy in which the immunosuppressive mechanism of one pathogen can be applied to attenuate a severe inflammation caused by another pathogen.
- Subjects
CANDIDA albicans; SEPSIS; LIPOPOLYSACCHARIDES; INTERLEUKIN-10; IMMUNOSUPPRESSION
- Publication
Communications Biology, 2021, Vol 4, Issue 1, p1
- ISSN
2399-3642
- Publication type
Article
- DOI
10.1038/s42003-021-01870-3