help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Published ahead of print on March 23, 2004, doi:10.1165/rcmb.2003-0285OC
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2003-0285OCv1
31/2/220    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Whittington, H. A.
Right arrow Articles by Millar, A. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Whittington, H. A.
Right arrow Articles by Millar, A. B.
American Journal of Respiratory Cell and Molecular Biology. Vol. 31, pp. 220-226, 2004
© 2004 American Thoracic Society
DOI: 10.1165/rcmb.2003-0285OC

Interleukin-22

A Potential Immunomodulatory Molecule in the Lung

Hayley A. Whittington, Lynne Armstrong, Kay M. Uppington and Ann B. Millar

Lung Research Group, Department of Clinical Sciences North Bristol, University of Bristol, Southmead Hospital, Westbury-on-Trym, Bristol, United Kingdom

Address correspondence to: Dr. Ann Millar, Lung Research Group, Dept of Clinical Sciences North Bristol, University of Bristol, Southmead Hospital, Westbury-on-Trym, Bristol BS10 5NB, UK. E-mail: ann.millar{at}bris.ac.uk

Interleukin (IL)-22 is a member of the human type I interferon family, which includes IL-10. IL-22 has the potential to interact with IL-10 because it binds to the IL-10R2c chain with IL-22R1 in its receptor complex. Binding can be blocked by the soluble receptor, IL-22 binding protein (IL-22BP). We hypothesize that IL-22 and IL-22BP are involved in inflammatory regulation and its subsequent role in the pathogenesis of inflammatory lung disease. We have demonstrated IL-22 mRNA expression in alveolar macrophages (AM), monocytes, and alveolar epithelial (AE) cells. IL-22BP mRNA is expressed in AM, AE cells, and neutrophils. In contrast, IL-22R1 is expressed in AE only. Immunohistochemistry on normal and interstitial lung disease lung sections has confirmed IL-22 protein expression. Western blotting for IL-22 in bronchoalveolar lavage fluid demonstrated that lower levels of IL-22 were present in patients with acute respiratory distress syndrome and sarcoidosis relative to control subjects (P = 0.0152 and P = 0.0213). Levels of IL-22 in idiopathic pulmonary fibrosis were not different than those of the control subjects (P = 0.5838). IL-22 did not affect IL-10 inhibition of tumor necrosis factor-{alpha} in monocytes, which do not express IL-22R1. By contrast, we demonstrated synergy between IL-10 and IL-22 in terms of IL-8 inhibition in IL-22R1-expressing A549 cells. These data suggest a role for IL-22 in the regulation of pulmonary inflammation.

Abbreviations: alveolar epithelial cells, AE • alveolar macrophages, AM • acute respiratory distress syndrome, ARDS • bronchoalveolar lavage, BAL • BAL fluid, BALF • glyceraldehyde-3-phosphate dehydrogenase, GAPDH • horseradish peroxidase, HRP • immunoglobulin, Ig • interleukin, IL • IL-10 receptor, IL-10R • IL-22 binding protein, IL-22BP • IL-22 receptor, IL-22R • interstitial lung disease, ILD • IL-10–related T cell–derived inducible factor, IL-TIF • idiopathic pulmonary fibrosis, IPF • lipopolysaccharide, LPS • reverse transcription polymerase chain reaction, RT-PCR • signal transducer activator of transcription, STAT • transforming growth factor-ß, TGF-ß • tumor necrosis factor-{alpha}, TNF-{alpha} • ventilated control, VC




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
W. Zhang, Y. Chen, H. Wei, C. Zheng, R. Sun, J. Zhang, and Z. Tian
Antiapoptotic Activity of Autocrine Interleukin-22 and Therapeutic Effects of Interleukin-22-Small Interfering RNA on Human Lung Cancer Xenografts
Clin. Cancer Res., October 15, 2008; 14(20): 6432 - 6439.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
E. Ziesche, M. Bachmann, H. Kleinert, J. Pfeilschifter, and H. Muhl
The Interleukin-22/STAT3 Pathway Potentiates Expression of Inducible Nitric-oxide Synthase in Human Colon Carcinoma Cells
J. Biol. Chem., June 1, 2007; 282(22): 16006 - 16015.
[Abstract] [Full Text] [PDF]


Home page
Infect. Immun.Home page
G. F. Weber, S. Schlautkotter, S. Kaiser-Moore, F. Altmayr, B. Holzmann, and H. Weighardt
Inhibition of Interleukin-22 Attenuates Bacterial Load and Organ Failure during Acute Polymicrobial Sepsis
Infect. Immun., April 1, 2007; 75(4): 1690 - 1697.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
H. Chang, H. Hanawa, H. Liu, T. Yoshida, M. Hayashi, R. Watanabe, S. Abe, K. Toba, K. Yoshida, R. Elnaggar, et al.
Hydrodynamic-Based Delivery of an Interleukin-22-Ig Fusion Gene Ameliorates Experimental Autoimmune Myocarditis in Rats
J. Immunol., September 15, 2006; 177(6): 3635 - 3643.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. Brand, F. Beigel, T. Olszak, K. Zitzmann, S. T. Eichhorst, J.-M. Otte, H. Diepolder, A. Marquardt, W. Jagla, A. Popp, et al.
IL-22 is increased in active Crohn's disease and promotes proinflammatory gene expression and intestinal epithelial cell migration
Am J Physiol Gastrointest Liver Physiol, April 1, 2006; 290(4): G827 - G838.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2004 American Thoracic Society.
  2009 ATS Conference