Analysis of IL-22 contribution to hepcidin induction and hypoferremia during the response to LPS in vivo

Wallace, Daniel F. and Subramaniam, V. Nathan (2015) Analysis of IL-22 contribution to hepcidin induction and hypoferremia during the response to LPS in vivo. International Immunology, 27 6: 281-287. doi:10.1093/intimm/dxu144


Author Wallace, Daniel F.
Subramaniam, V. Nathan
Title Analysis of IL-22 contribution to hepcidin induction and hypoferremia during the response to LPS in vivo
Formatted title
Analysis of IL-22 contribution to hepcidin induction and hypoferremia during the response to LPS in vivo
Journal name International Immunology   Check publisher's open access policy
ISSN 1460-2377
0953-8178
Publication date 2015-06-01
Year available 2015
Sub-type Article (original research)
DOI 10.1093/intimm/dxu144
Open Access Status Not Open Access
Volume 27
Issue 6
Start page 281
End page 287
Total pages 7
Place of publication Oxford, United Kingdom
Publisher Oxford University Press
Language eng
Formatted abstract
The anaemia of chronic disease (ACD) results from inflammation-mediated up-regulation of the iron regulatory hormone hepcidin, with the consequent sequestration of iron limiting its availability for erythropoiesis. The inflammatory cytokine IL-6, a regulator of hepcidin, has been implicated in this process. Recent in vivo and in vitro studies indicate that IL-22 is also able to stimulate hepcidin expression. We aimed to determine if IL-22 had a role in causing the hypoferremia associated with the inflammatory response. Wild-type and Il22-knockout mice were subjected to an acute inflammatory stimulus via administration of LPS and the response of hepcidin and iron homeostasis was analysed. In the absence of IL-22, there was a response of hepcidin, resulting in a reduction in serum iron levels. However, the hypoferremic response to LPS was slightly blunted in mice lacking IL-22, suggesting that, during LPS-mediated inflammation, IL-22 may play a minor role in mediating the hypoferremic response. These results may have implications for the treatment and management of the ACD.
Keyword Anaemia of chronic disease
Hepcidin
IL-22
Inflammation
Iron
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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