The Effects of IL-22 on the Inflammatory Mediator Production, Proliferation, and Barrier Function of HUVECs

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.

Interleukin-22 promotes tumor angiogenesis

“…Here, we observed that human endothelial cells express IL-22R, suggesting that like IL-17, IL-22 may play a role in angiogenesis. Further support of this notion was recently provided by He et al, who reported that treating HUVECs with IL-22 caused an increase in proliferation, and Wu et al who observed a pro-survival effect of IL-22 on pulmonary microvascular cells in a model of lung injury [29,30]. We observed similar effects by IL-22 under high and low serum concentrations, respectively.…”

HClO‐Activated Near‐Infrared Fluorogenic Aza‐BODIPY‐Bisferrocene Triad with High Turn‐on Ratio for In Vivo Biosensing

“…HUVEC cells were pretreated with lipopolysaccharide (LPS) for 4 h to generate endogenous ClO – . [ 28 ] Imaging Fc 2 ‐CBDP micelles showed that LPS‐treated cells exhibited ≈16‐fold signal enhancement than the untreated control (Figure 3c,e). Furthermore, after pretreating HUVEC cells with N ‐acetyl‐ L ‐cysteine (NAC; 1 m m ) as a ROS scavenger for 2 h, [ 3a ] the signal enhancement ratio only reached to ≈fourfold as compared with the LPS‐untreated control (Figure 3e).…”

Interleukin-22 Immunotherapy during Severe Influenza Enhances Lung Tissue Integrity and Reduces Secondary Bacterial Systemic Invasion

“…Under resting conditions, the IL-22 receptor (IL-22R1 subunit) mainly locates on tracheobronchial epithelial cells and, to a lesser extent, on airway epithelial cells (large and small airways, but not parenchyma) (52). Of interest, recent data indicate that the IL-22 receptor is also expressed by (microvascular) endothelial cells, especially at alveolar sites (60,61). Although it has been suggested that neutrophil proteolytic enzymes might cleave the IL-22 receptor (62), its expression appears to increase during the course of influenza (at least at 21 days postinfection) to localize at the sites of parenchymal lung remodeling/repair (repairing alveoli) (52).…”