Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo

E. Ziesché, P. Scheiermann, M. Bachmann, C. D. Sadik, C. Hofstetter, B. Zwissler, J. Pfeilschifter, H. Mühl*

*Corresponding author for this work
23 Citations (Scopus)


Summary 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.

Original languageEnglish
JournalClinical and Experimental Immunology
Issue number3
Pages (from-to)370-376
Number of pages7
Publication statusPublished - 01.09.2009


Dive into the research topics of 'Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo'. Together they form a unique fingerprint.

Cite this