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Immune Resolution Dilemma: Host Antimicrobial Factor S100A8/A9 Modulates Inflammatory Collateral Tissue Damage During Disseminated Fungal Peritonitis
Umeå University, Faculty of Medicine, Department of Clinical Microbiology. Umeå University, Faculty of Medicine, Umeå Centre for Microbial Research (UCMR). Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS).
Umeå University, Faculty of Medicine, Department of Clinical Microbiology. Umeå University, Faculty of Medicine, Umeå Centre for Microbial Research (UCMR). Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS).
Umeå University, Faculty of Medicine, Department of Clinical Microbiology. Umeå University, Faculty of Medicine, Umeå Centre for Microbial Research (UCMR). Umeå University, Faculty of Medicine, Molecular Infection Medicine Sweden (MIMS).
Umeå University, Faculty of Medicine, Department of Medical Biochemistry and Biophysics.
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2021 (English)In: Frontiers in Immunology, E-ISSN 1664-3224, Vol. 12, article id 553911Article in journal (Refereed) Published
Abstract [en]

Intra-abdominal infection (peritonitis) is a leading cause of severe disease in surgical intensive care units, as over 70% of patients diagnosed with peritonitis develop septic shock. A critical role of the immune system is to return to homeostasis after combating infection. S100A8/A9 (calprotectin) is an antimicrobial and pro-inflammatory protein complex used as a biomarker for diagnosis of numerous inflammatory disorders. Here we describe the role of S100A8/A9 in inflammatory collateral tissue damage (ICTD). Using a mouse model of disseminated intra-abdominal candidiasis (IAC) in wild-type and S100A8/A9-deficient mice in the presence or absence of S100A9 inhibitor paquinimod, the role of S100A8/A9 during ICTD and fungal clearance were investigated. S100A8/A9-deficient mice developed less ICTD than wild-type mice. Restoration of S100A8/A9 in knockout mice by injection of recombinant protein resulted in increased ICTD and fungal clearance comparable to wild-type levels. Treatment with paquinimod abolished ICTD and S100A9-deficient mice showed increased survival compared to wild-type littermates. The data indicates that S100A8/A9 controls ICTD levels and antimicrobial activity during IAC and that targeting of S100A8/A9 could serve as promising adjunct therapy against this challenging disease.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2021. Vol. 12, article id 553911
Keywords [en]
Candida albicans, host-pathogen interactions, host-targeted agents, inflammation, peritonitis, S100A8/A9 complex, sepsis
National Category
Immunology in the medical area
Identifiers
URN: urn:nbn:se:umu:diva-181798DOI: 10.3389/fimmu.2021.553911ISI: 000627778800001Scopus ID: 2-s2.0-85102439343OAI: oai:DiVA.org:umu-181798DiVA, id: diva2:1541456
Funder
The Kempe Foundations, SMK-1453Swedish Research Council, VR-M 2017-01681Swedish Research Council, 2014-02281Available from: 2021-04-01 Created: 2021-04-01 Last updated: 2024-01-17Bibliographically approved

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Shankar, MadhuUwamahoro, NathalieBackman, EmelieHolmberg, SandraNiemiec, Maria JoannaUrban, Constantin F.

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Shankar, MadhuUwamahoro, NathalieBackman, EmelieHolmberg, SandraNiemiec, Maria JoannaUrban, Constantin F.
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Department of Clinical MicrobiologyUmeå Centre for Microbial Research (UCMR)Molecular Infection Medicine Sweden (MIMS)Department of Medical Biochemistry and Biophysics
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