Low sensitivity to glucocorticoid inhibition of in vitro Th17-related cytokine production in multiple sclerosis patients is related to elevated plasma lipopolysaccharide levels

Copyright © 2013 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 148(2013), 2 vom: 15. Aug., Seite 209-18
1. Verfasser: Teixeira, Bruna (VerfasserIn)
Weitere Verfasser: Bittencourt, Vera Carolina B, Ferreira, Thais B, Kasahara, Taissa M, Barros, Priscila O, Alvarenga, Regina, Hygino, Joana, Andrade, Regis M, Andrade, Arnaldo F, Bento, Cleonice A M
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2013
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't CD8(+) T cells Cytokines; IL-10; Lipopolysaccharide; Multiple sclerosis; Th17; Cytokines Glucocorticoids mehr... Lipopolysaccharides Hydrocortisone WI4X0X7BPJ
Beschreibung
Zusammenfassung:Copyright © 2013 Elsevier Inc. All rights reserved.
Exogenous glucocorticoid plays an important role in controlling clinical relapses of multiple sclerosis (MS), but the response to this treatment differs among patients. In this study, T-cell proliferation and IL-17 production were less sensitive to hydrocortisone (HC) inhibition in MS patients than healthy individuals, mainly in CD8(+) compartment. Furthermore, in vitro IL-17 production was positively related with neurological disability and its release was proportional to IL-23 and IL-6 productions by LPS-activated monocytes. Interestingly, elevated LPS levels were quantified in the plasma of MS patients, and their levels were directly related to in vivo IL-6 production. Finally, HC-resistance in reducing IL-17 production by polyclonally-activated CD8(+) T cells was particularly observed among MS patients with higher in vivo LPS levels. In summary, the results indicate that T-cells derived from MS patients show an enhanced Th17-like phenotype that is directly associated with neurological disability, resistance to glucocorticoid inhibition and elevated bacterial translocation
Beschreibung:Date Completed 17.09.2013
Date Revised 21.11.2013
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2013.05.012