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      Cell wall N-glycan of Candida albicans ameliorates early hyper- and late hypo-immunoreactivity in sepsis

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          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.

          Abstract

          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.

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          Most cited references34

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          Sepsis and septic shock

          Sepsis is a common condition that is associated with unacceptably high mortality and, for many of those who survive, long-term morbidity. Increased awareness of the condition resulting from ongoing campaigns and the evidence arising from research in the past 10 years have increased understanding of this problem among clinicians and lay people, and have led to improved outcomes. The World Health Assembly and WHO made sepsis a global health priority in 2017 and have adopted a resolution to improve the prevention, diagnosis, and management of sepsis. In 2016, a new definition of sepsis (Sepsis-3) was developed. Sepsis is now defined as infection with organ dysfunction. This definition codifies organ dysfunction using the Sequential Organ Failure Assessment score. Ongoing research aims to improve definition of patient populations to allow for individualised management strategies matched to a patient's molecular and biochemical profile. The search continues for improved diagnostic techniques that can facilitate this aim, and for a pharmacological agent that can improve outcomes by modifying the disease process. While waiting for this goal to be achieved, improved basic care driven by education and quality-improvement programmes offers the best hope of increasing favourable outcomes.
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            Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy.

            Sepsis - which is a severe life-threatening infection with organ dysfunction - initiates a complex interplay of host pro-inflammatory and anti-inflammatory processes. Sepsis can be considered a race to the death between the pathogens and the host immune system, and it is the proper balance between the often competing pro- and anti-inflammatory pathways that determines the fate of the individual. Although the field of sepsis research has witnessed the failure of many highly touted clinical trials, a better understanding of the pathophysiological basis of the disorder and the mechanisms responsible for the associated pro- and anti-inflammatory responses provides a novel approach for treating this highly lethal condition. Biomarker-guided immunotherapy that is administered to patients at the proper immune phase of sepsis is potentially a major advance in the treatment of sepsis and in the field of infectious disease.
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              The immunopathology of sepsis and potential therapeutic targets

              Sepsis — which is caused by a dysregulated host response to infection — is a life-threatening organ dysfunction. This Review describes the recent advances in our understanding of sepsis pathogenesis and discusses strategies for the development of successful therapies.
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                Author and article information

                Contributors
                ktakahar@zoo.zool.kyoto-u.ac.jp
                Journal
                Commun Biol
                Commun Biol
                Communications Biology
                Nature Publishing Group UK (London )
                2399-3642
                16 March 2021
                16 March 2021
                2021
                : 4
                : 342
                Affiliations
                [1 ]GRID grid.258799.8, ISNI 0000 0004 0372 2033, Department of Animal Development and Physiology, Graduate School of Biostudies, , Kyoto University, ; Kyoto, Japan
                [2 ]GRID grid.258799.8, ISNI 0000 0004 0372 2033, Laboratory of Immune Regulation, Department of Virus Research, Institute for Frontier Life and Medical Sciences, , Kyoto University, ; Kyoto, Japan
                [3 ]GRID grid.258799.8, ISNI 0000 0004 0372 2033, Graduate School of Medicine, , Kyoto University, ; Kyoto, Japan
                [4 ]GRID grid.412755.0, ISNI 0000 0001 2166 7427, Division of Infection and Host Defense, , Tohoku Medical and Pharmaceutical University, ; Sendai, Japan
                [5 ]GRID grid.174567.6, ISNI 0000 0000 8902 2273, Biomolecular Chemistry Laboratory, Graduate School of Engineering, , Nagasaki University, ; Nagasaki, Japan
                Author information
                http://orcid.org/0000-0003-1825-8512
                http://orcid.org/0000-0002-6822-4137
                http://orcid.org/0000-0002-9757-1939
                http://orcid.org/0000-0002-2707-1947
                http://orcid.org/0000-0001-6372-7563
                http://orcid.org/0000-0002-9505-1980
                http://orcid.org/0000-0003-4730-8187
                Article
                1870
                10.1038/s42003-021-01870-3
                7966402
                33727664
                702b043f-b481-4c1e-9286-0bade4071ef5
                © The Author(s) 2021

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 26 June 2020
                : 11 February 2021
                Funding
                Funded by: 1) Grant-in-Aid for Scientific Research (16K08737 to KT) from the Ministry of Education, Science, Sports and Culture of Japan. 2)The Kyoto University Foundation (to KT) 3) GAP fund program (to KT) from Kyoto University Research Development Program 4) ISHIZUE 2019 from Kyoto University Research Development Program (to KT).
                Categories
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                Custom metadata
                © The Author(s) 2021

                sepsis,immune evasion
                sepsis, immune evasion

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