Published ahead of print on March 23, 2004, doi:10.1165/rcmb.2003-0285OC
© 2004 American Thoracic Society DOI: 10.1165/rcmb.2003-0285OC Interleukin-22A Potential Immunomodulatory Molecule in the LungLung 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-
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- This article has been cited by other articles:
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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. 
