MHC/class-II-positive cells inhibit corticosterone of adrenal gland cells in experimental arthritis: a role for IL-1 beta, IL-18, and the inflammasome

Stangl, Hubert and Krammetsvogl, Anita and Lesiak, Martin and Wolff, Christine and Straub, Rainer H. (2020) MHC/class-II-positive cells inhibit corticosterone of adrenal gland cells in experimental arthritis: a role for IL-1 beta, IL-18, and the inflammasome. SCIENTIFIC REPORTS, 10 (1): 17071. ISSN 2045-2322,

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Abstract

In experimental arthritis, glucocorticoid secretion is inadequate relative to inflammation. We hypothesized that IL-1 is a key factor for inadequate glucocorticoid secretion in arthritic rats. Collagen type II-induced arthritis (CIA) in DA rats was the model to study effects of IL-1 on adrenal function. In the CIA model, an increase of intraadrenal MHCII-positive cells was observed. MHCII-positive cells or bone marrow-derived dendritic cells inhibited glucocorticoid secretion of adrenal gland cells. IL-1, but also IL-18 and the inflammasome were critical in glucocorticoid inhibition. Arthritic compared to control adrenal gland cells produced higher amounts of CXC chemokines from MHCII+ adrenal cells, particularly CINC-2, which is strongly dependent on presence of IL-1. In CIA, macrophages and/or dendritic cells inhibit glucocorticoid secretion via IL-1 in adrenal glands. These findings show that activated macrophages and/or dendritic cells inhibit glucocorticoid secretion in experimental arthritis and that IL-1 beta is a decisive factor.

Item Type: Article
Uncontrolled Keywords: TUMOR-NECROSIS-FACTOR; DENDRITIC CELLS; RHEUMATOID-ARTHRITIS; CORTISOL PRODUCTION; IMMUNE-SYSTEM; CYTOKINES; AXIS; ADRENOCORTICOTROPIN; INTERLEUKIN-6; EXPRESSION;
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin I
Depositing User: Dr. Gernot Deinzer
Date Deposited: 09 Mar 2021 06:28
Last Modified: 09 Mar 2021 06:28
URI: https://pred.uni-regensburg.de/id/eprint/43567

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