- Inflammation regulates 11 beta-hydroxysteroid dehydrogenase type 1 di…
Počet záznamů: 1  

Inflammation regulates 11 beta-hydroxysteroid dehydrogenase type 1 differentially in specific compartments of the gut mucosal immune system

  1. 1.
    SYSNO ASEP0479728
    Druh ASEPJ - Článek v odborném periodiku
    Zařazení RIVJ - Článek v odborném periodiku
    Poddruh JČlánek ve WOS
    NázevInflammation regulates 11 beta-hydroxysteroid dehydrogenase type 1 differentially in specific compartments of the gut mucosal immune system
    Tvůrce(i) Ergang, Peter (FGU-C) RID, ORCID
    Vodička, Martin (FGU-C) RID, ORCID, SAI
    Vagnerová, Karla (FGU-C) RID, ORCID
    Moravec, Martin (FGU-C)
    Kvapilová, Pavlína (FGU-C)
    Kment, M. (CZ)
    Pácha, Jiří (FGU-C) RID, ORCID
    Zdroj.dok.Steroids. - : Elsevier - ISSN 0039-128X
    Roč. 126, Oct 2017 (2017), s. 66-73
    Poč.str.8 s.
    Jazyk dok.eng - angličtina
    Země vyd.US - Spojené státy americké
    Klíč. slovametabolism of glucocorticoids ; cytokine microenvironment ; lymphoid organs ; colon ; Dextran sodium sulfate colitis
    Vědní obor RIVED - Fyziologie
    Obor OECDPhysiology (including cytology)
    CEPGAP303/10/0969 GA ČR - Grantová agentura ČR
    GA15-07268S GA ČR - Grantová agentura ČR
    Institucionální podporaFGU-C - RVO:67985823
    UT WOS000411539400009
    EID SCOPUS85028049692
    DOI https://doi.org/10.1016/j.steroids.2017.07.007
    AnotaceThe bioavailability of glucocorticoids is modulated by enzyme 11 beta-hydroxysteroid dehydrogenase type 1 (11HSD1), which catalyzes the conversion of inactive 11-oxo-glucocorticoids to active 11-hydroxy-glucocorticoids cortisol and corticosterone and is regulated by pro-inflammatory cytokines. Our aim was to assess the effect of colitis on the expression of 11HSD1 in specific microanatomical compartments of the mucosal immune system. Using qRT-PCR we quantified the expression of 11HSD1 and cytokines in the colon, mesenteric lymph nodes (MLN) and spleen of mice with colitis. Microsamples of the MLN cortex, paracortex and medulla, colonic crypt epithelium (CCE), lamina propria and isolated intestinal lymphoid follicles (ILF) were harvested by laser microdissection, whereas splenic and MLN lymphocytes by flow cytometry. Colitis increased 11HSD1 in the CCE, ILF, and MLN cortex but not in the lamina propria and the MLN paracortex and medulla. Expression of IL-4, IL-21 and TNFa was increased in both the cortex of MLN and ILF, whereas IL-1 beta and IL-10 were only increased in the follicles. No positive effect was observed in the case of IFN gamma and TGF beta. 11HSD1 was positively correlated with TNFa and less strongly with IL-21, IL-1 beta, and IL-4. Colitis also upregulated the 11HSD1 expression of T cells in the spleen and MLN. The study demonstrates the stimulatory effect of inflammation on local glucocorticoid metabolism only in particular compartments of the mucosal immune system. The correlation between cytokines and 11HSD1 in the ILF and MLN cortex indicates that pro-inflammatory cytokines may amplify glucocorticoid signals in inductive compartments of the mucosal immune system.
    PracovištěFyziologický ústav
    KontaktLucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400
    Rok sběru2018
Počet záznamů: 1  

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