The Effects of IL-22 on the Inflammatory Mediator Production, Proliferation, and Barrier Function of HUVECs
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ORIGINAL ARTICLE
The Effects of IL-22 on the Inflammatory Mediator Production, Proliferation, and Barrier Function of HUVECs Xian He,1 Hui Li,1 Ying Chen,1 Aijun Chen,1 Kui Shan,1 Jin Chen,1 Hengguang Zhao,1 Xiaojiao Zhang,1 and Tao Cai1,2
Abstract—The aim of this study was to investigate the effects of interleukin (IL)-22 on proliferation function and inflammatory mediator production and barrier function of human umbilical vein endothelial cells (HUVECs). The expression of mRNA was detected by RT-PCR. The proliferation ability of cells was evaluated using a cell counting kit assay. Real-time quantitative PCR and Western blot were used to detect the expression of inflammatory mediators. The endothelial barrier permeability was assessed by measuring permeability to FITC-labeled dextran. The distribution of occludin was detected by immunofluorescence. IL-22R1 mRNA expression was noted in HUVECs. IL-22 could enhance the proliferation ability of HUVECs and suppress lipopolysaccharide (LPS)-induced proliferation inhibition in these cells. IL-22 also enhanced the production of CCL2 and CCL20 by HUVECs. Besides, IL-22 could improve barrier function and decrease LPS-induced increased cellular permeability and inhibit the LPS-induced destruction of occludin in HUVECs. IL-22 may play a protective role in the development of vasculitis. KEY WORDS: Behcet syndrome; IL-22; inflammatory; LPS; vasculitis.
INTRODUCTION Interleukin (IL)-22 is a member of the IL-10 superfamily, which is primarily produced by activated T cells and natural killer cells [1]. It has been known to mediate its effect through the following two receptors: IL-10Rb, which is ubiquitously expressed, and the heterodimeric receptor IL22R1, which is restricted to nonlymphoid cells, with a high level of expression in the pancreas, kidney, and liver, as well as barrier surfaces such as the skin, intestine, and lungs [2– 4]. Recent studies have shown that increased expression of IL-22 and genetic polymorphisms in IL-22 are associated with several inflammatory diseases. Expression of IL-22 can provide direct tissue-protective effects on various nonhematopoietic cellular targets during inflammation, such 1
The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China 2 To whom correspondence should be addressed at The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China. E-mail: [email protected]
as the liver, bowel, heart, and lungs [5–10]. Nevertheless, IL-22 expression is not always constitutively tissue protective in inflammatory diseases. Other studies demonstrated that IL-22 also participates in the pathogenesis of inflammatory diseases as a proinflammatory factor, such as bleomycin-induced acute airway damage, autoimmune thyroid diseases, and West Nile encephalitis [11–13]. Collectively, these studies demonstrated that IL-22 expression has been found to contribute to either proinflammatory or tissueprotective phases of immune response depending on the context in which it is
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