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Interleukin-22: a potential immunomodulatory molecule in the lung
Hayley A Whittington1, Lynne Armstrong, Kay M Uppington
1Lung Research Group, Department of Clinical Sciences North Bristol, University of Bristol, Southmead Hospital, Westbury-on-Trym, Bristol BS10 5NB, UK.
American Journal of Respiratory Cell and Molecular Biology
|March 25, 2004
Summary
Interleukin-22 (IL-22) plays a role in regulating lung inflammation. Lower IL-22 levels were observed in patients with acute respiratory distress syndrome and sarcoidosis, suggesting its involvement in inflammatory lung diseases.
Area of Science:
- Immunology
- Pulmonary Medicine
- Molecular Biology
Background:
- Interleukin-22 (IL-22) is part of the type I interferon family, sharing characteristics with IL-10.
- IL-22 interacts with IL-10 receptor subunit 2 (IL-10R2c) and IL-22 receptor 1 (IL-22R1), with binding inhibited by IL-22 binding protein (IL-22BP).
- IL-22 and IL-22BP are hypothesized to be involved in inflammatory regulation and the pathogenesis of inflammatory lung diseases.
Purpose of the Study:
- To investigate the expression and function of IL-22 and IL-22BP in the context of pulmonary inflammation.
- To determine the role of IL-22 in inflammatory lung diseases such as acute respiratory distress syndrome (ARDS), sarcoidosis, and idiopathic pulmonary fibrosis (IPF).
Main Methods:
- Assessed mRNA expression of IL-22, IL-22BP, and IL-22R1 in various lung cells (alveolar macrophages, monocytes, alveolar epithelial cells, neutrophils).
- Utilized immunohistochemistry to confirm IL-22 protein expression in lung tissues.
- Quantified IL-22 levels in bronchoalveolar lavage fluid from patients with ARDS, sarcoidosis, IPF, and healthy controls using Western blotting.
- Evaluated the functional interaction of IL-22 and IL-10 on cytokine inhibition (TNF-alpha and IL-8) in relevant cell lines.
Main Results:
- IL-22 mRNA was detected in alveolar macrophages, monocytes, and alveolar epithelial cells.
- IL-22BP mRNA was found in alveolar macrophages, alveolar epithelial cells, and neutrophils, while IL-22R1 was exclusively expressed in alveolar epithelial cells.
- Lower IL-22 protein levels were found in bronchoalveolar lavage fluid of patients with ARDS and sarcoidosis compared to controls.
- IL-22 did not influence IL-10's inhibition of TNF-alpha in monocytes but showed synergistic IL-8 inhibition with IL-10 in IL-22R1-expressing A549 cells.
Conclusions:
- IL-22 is expressed in key pulmonary cells and its protein levels are altered in specific inflammatory lung conditions.
- The differential expression of IL-22 receptor components suggests cell-specific functions.
- IL-22, in conjunction with IL-10, can modulate inflammatory responses, particularly IL-8 production, in cells expressing IL-22R1, indicating a regulatory role in pulmonary inflammation.
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