Inflammation regulates 11β-hydroxysteroid dehydrogenase type 1 differentially in specific compartments of the gut mucosal immune system
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
28754259
DOI
10.1016/j.steroids.2017.07.007
PII: S0039-128X(17)30121-6
Knihovny.cz E-zdroje
- Klíčová slova
- Colon, Cytokine microenvironment, Dextran sodium sulfate colitis, Lymphoid organs, Metabolism of glucocorticoids,
- MeSH
- 11-beta-hydroxysteroiddehydrogenasa typ 1 genetika metabolismus MeSH
- cytokiny metabolismus MeSH
- kolitida enzymologie genetika imunologie MeSH
- myši inbrední BALB C MeSH
- myši MeSH
- regulace genové exprese enzymů MeSH
- střevní sliznice imunologie MeSH
- zánět enzymologie genetika imunologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 11-beta-hydroxysteroiddehydrogenasa typ 1 MeSH
- cytokiny MeSH
The bioavailability of glucocorticoids is modulated by enzyme 11β-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 TNFα was increased in both the cortex of MLN and ILF, whereas IL-1β and IL-10 were only increased in the follicles. No positive effect was observed in the case of IFNγ and TGFβ. 11HSD1 was positively correlated with TNFα and less strongly with IL-21, IL-1β, 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.
2nd Department of Internal Medicine 3rd Faculty of Medicine Charles University Prague Czech Republic
Institute of Physiology Academy of Sciences of the Czech Republic Prague Czech Republic
Citace poskytuje Crossref.org
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