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Interleukin-18, IL-18 binding protein and IL-18 receptor expression in asthma: a hypothesis showing IL-18 promotes
Davinder Kaur1, Latifa Chachi1, Edith Gomez1
1Department of Respiratory Sciences Institute for Lung Health NIHR Biomedical Research Centre University of Leicester Leicester LE1 7RH UK.
Objective:
In asthma, genome-wide association studies have shown that interleukin-18 (IL-18) receptor 1 gene (IL-18R1) and sputum IL-18 are increased during exacerbations. However, the role of the IL-18 axis in bronchial epithelial function is unclear. To investigate IL-18, IL-18 binding protein (BP) and IL-18R expression in bronchial biopsies and sputum samples from patients with asthma, and to determine its functional role using in vitro bronchial epithelial cells.
Methods:
The expression of IL-18, IL-18BP and IL-18Rα was examined in subjects with asthma and healthy controls in bronchial biopsies by immunohistochemistry and IL-18 and IL-18BP release in sputum. In epithelial cells, the mRNA and protein expression of IL-18, IL-18BP, IL-18Rα and IL-18Rβ was assessed by qPCR, flow cytometry, Western blotting and immunofluorescence respectively. IL-18 function in epithelial cells was examined by intracellular calcium, wound repair, synthetic activation and epithelial differentiation changes.
Results:
In biopsies from subjects with asthma, the IL-18 expression was not different in the lamina propria compared with controls but was decreased in the epithelium. In contrast, the IL-18BP was decreased in the lamina propria in asthma and was absent in the bronchial epithelium. IL-18 was released in sputum with IL-18BP elevated in patients with asthma. The IL-18Rα expression was not different between health and disease. In vitro, IL-18-stimulated bronchial epithelial cells increased intracellular calcium, wound repair, metabolic activity, morphological changes and epithelial cellular differentiation.
Conclusion:
In asthma, the dynamic interaction between IL-18, its cognate receptor and natural inhibitor is complex, with differences between airway compartments. Upregulation of IL-18 can promote epithelial activation and cellular differentiation.
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