Cortisol metabolism by 11β‐hydroxysteroid dehydrogenase as a novel target in the treatment of inflammation‐ or immune‐mediated bone loss: Comment on the article by Makrygiannakis et al

Wilckens, Thomas; Volkmann, Ariane

doi:10.1002/art.22318

Cited by 2 publications

(1 citation statement)

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“…It is unknown whether and how endogenous glucocorticoids (GC) contribute to the initiation and maintenance of rheumatoid arthritis (RA) and other inflammatory diseases [1-7]. We previously studied the role of endogenous GC in the K/BxN serum-induced arthritis mouse model of RA [8].…”

Section: Introductionmentioning

confidence: 99%

Acute murine antigen-induced arthritis is not affected by disruption of osteoblastic glucocorticoid signalling

Spies

Wiebe

et al. 2014

BMC Musculoskelet Disord

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BackgroundThe role of endogenous glucocorticoids (GC) in the initiation and maintenance of rheumatoid arthritis (RA) remains unclear. We demonstrated previously that disruption of GC signalling in osteoblasts results in a profound attenuation of K/BxN serum-induced arthritis, a mouse model of RA. To determine whether or not the modulation of the inflammatory response by osteoblasts involves T cells, we studied the effects of disrupted osteoblastic GC-signalling in the T cell-dependent model of antigen-induced arthritis (AIA).MethodsAcute arthritis was induced in pre-immunised 11-week-old male 11β-hydroxysteroid dehydrogenase type 2 transgenic (tg) mice and their wild-type (WT) littermates by intra-articular injection of methylated bovine serum albumine (mBSA) into one knee joint. Knee diameter was measured every 1–2 days until euthanasia on day 14 post injection. In a separate experiment, arthritis was maintained for 28 days by weekly reinjections of mBSA. Tissues were analysed by histology, histomorphometry and microfocal-computed tomography. Serum cytokines levels were determined by multiplex suspension array.ResultsIn both short and long term experiments, arthritis developed in tg and WT mice with no significant difference between both groups. Histological indices of inflammation, cartilage damage and bone erosion were similar in tg and WT mice. Bone volume and turnover at the contralateral tibia and systemic cytokine levels were not different.ConclusionsAcute murine AIA is not affected by a disruption in osteoblastic GC signalling. These data indicate that osteoblasts do not modulate the T cell-mediated inflammatory response via a GC-dependent pathway.

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Section: Introductionmentioning

confidence: 99%

Acute murine antigen-induced arthritis is not affected by disruption of osteoblastic glucocorticoid signalling

Spies

Wiebe

et al. 2014

BMC Musculoskelet Disord

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Glucocorticoids

Spies

Strehl

Goes

et al. 2011

Best Practice & Research Clinical Rheumatology

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Glucocorticoids remain part of the treatment strategy in many rheumatic diseases, because of their anti-inflammatory and immunosuppressive actions. Unfortunately, their clinically desired effects are linked to adverse effects, especially at higher dosages and longer duration of treatment. In this review, we describe new insights into the mechanisms of anti-inflammatory glucocorticoid actions and provide an update on recent approaches to improve the risk/benefit ratio of glucocorticoid therapy. Improved knowledge of the immunomodulatory role of endogenous glucocorticoids has evolved, and we report on the therapeutic potential of targeting glucocorticoid pre-receptor metabolism for metabolic and inflammatory diseases.

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Cortisol metabolism by 11β‐hydroxysteroid dehydrogenase as a novel target in the treatment of inflammation‐ or immune‐mediated bone loss: Comment on the article by Makrygiannakis et al

Cited by 2 publications

References 8 publications

Acute murine antigen-induced arthritis is not affected by disruption of osteoblastic glucocorticoid signalling

Acute murine antigen-induced arthritis is not affected by disruption of osteoblastic glucocorticoid signalling

Glucocorticoids

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