Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo
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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.
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Systemic use of dexamethasone can cause serious side-effects by depressing the innate immune response and increasing infection likelihood.
“systemic use of DX can cause serious side-effects by depressing the innate immune response, thus increasing the likelihood of infection.178–179”
From Biocompatible Materials for Continuous Glucose Monitoring Devices (2013) · cites this paper as [178]
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Biocompatible Materials for Continuous Glucose Monitoring Devices
Nichols, S. P., Koh, A., Storm, W. L., Shin, J. H., & Schoenfisch, M. H. (2013) · Chemical Reviews · doi:10.1021/cr300387j · Cited by 347 · see citing works
- Authors
- Ziesché, E., Scheiermann, P., Bachmann, M., Sadik, C. D., Hofstetter, C., Zwissler, B., Pfeilschifter, J., & Mühl, H.
- Affiliations
- Goethe University Frankfurt (DE)
- Ludwig-Maximilians-Universität München (DE)
- Pharmazentrum Frankfurt/ZAFES
- Corresponding author
- Mühl, H
- Venue
- Clinical and Experimental Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-05-06
- Volume
- 157
- Issue
- 3
- Pages
- 370-376
- ISSN
- 0009-9104 (ISSN-L)
- 1365-2249
- PMC
- PMC2745031
- OpenAlex
- W1540737922
- Cited by
- 40
- References
- 34
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 4 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 5 · 2013: 5 · 2012: 4
- FWCI
- 1.75
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Clinical & Experimental Immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- dexamethasone, IL-22, glucocorticoids, bacterial infection, sepsis, Staphylococcus epidermidis, innate immunity, Crohn's disease, corticosteroid therapy, bacterial translocation, peripheral blood mononuclear cells, intestinal epithelial damage
- MeSH terms
- Interleukin-22, Animals, Cells, Cultured, Depression, Chemical, Dexamethasone, Glucocorticoids, Humans, Interleukins, Male, Peritonitis, Random Allocation, RNA, Messenger, Staphylococcal Infections, Staphylococcus epidermidis, Gene Expression, Case-Control Studies, Interleukin-8, Interleukin-10, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Models, Animal, Rats
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