These authors contributed equally to this work.
Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo
Article first published online: 6 MAY 2009
© 2009 British Society for Immunology
Clinical & Experimental Immunology
Volume 157, Issue 3, pages 370–376, September 2009
How to Cite
Ziesché, E., Scheiermann, P., Bachmann, M., Sadik, C. D., Hofstetter, C., Zwissler, B., Pfeilschifter, J. and Mühl, H. (2009), Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo. Clinical & Experimental Immunology, 157: 370–376. doi: 10.1111/j.1365-2249.2009.03969.x
- Issue published online: 27 JUL 2009
- Article first published online: 6 MAY 2009
- Accepted for publication 27 April 2009
Interleukin (IL)-22 production triggered by innate immune mechanisms has been identified as key to efficient intestinal anti-bacterial host defence and preservation of homeostasis. We hypothesized that glucocorticoid therapy may impair IL-22 expression, which should promote intestinal epithelial damage with the potential of subsequent bacterial translocation. High-dose corticosteroid therapy in Crohn's disease has been associated with an increased rate of abscess formation and ultimately with a higher risk of developing postoperative infectious complications, including abdominal sepsis. Thus, we sought to investigate effects of the prototypic glucocorticoid dexamethasone on IL-22 production in the context of bacterial infection. Enhanced IL-22 plasma levels were detectable in rat sepsis. Moreover, heat-inactivated Staphylococcus epidermidis, used as a prototypic activator of innate immunity, induced robust production of IL-22 by human peripheral blood mononuclear cells (PBMC). Here, we report for the first time that dexamethasone mediates remarkable suppression of IL-22 as detected in S. epidermidis-activated PBMC and rat sepsis, respectively. The data presented herein suggest that insufficient IL-22 function may contribute to impaired intestinal host defence in the context of corticosteroid therapy.