| First Author | Lee D | Year | 2022 |
| Journal | Int J Mol Sci | Volume | 23 |
| Issue | 2 | PubMed ID | 35054942 |
| Mgi Jnum | J:322473 | Mgi Id | MGI:6861284 |
| Doi | 10.3390/ijms23020757 | Citation | Lee D, et al. (2022) The Roles of IL-22 and Its Receptor in the Regulation of Inflammatory Responses in the Brain. Int J Mol Sci 23(2) |
| abstractText | Interleukin (IL)-22 is a potent mediator of inflammatory responses. The IL-22 receptor consists of the IL-22Ralpha and IL-10Rbeta subunits. Previous studies have shown that IL-22Ralpha expression is restricted to non-hematopoietic cells in the skin, pancreas, intestine, liver, lung, and kidney. Although IL-22 is involved in the development of inflammatory responses, there have been no reports of its role in brain inflammation. Here, we used RT-PCR, Western blotting, flow cytometry, immunohistochemical, and microarray analyses to examine the role of IL-22 and expression of IL-22Ralpha in the brain, using the microglial cell line, hippocampal neuronal cell line, and inflamed mouse brain tissue. Treatment of BV2 and HT22 cells with recombinant IL-22 increased the expression levels of the pro-inflammatory cytokines IL-6 and TNF-alpha, as well as cyclooxygenase (COX)-2 and prostaglandin E2. We also found that the JNK and STAT3 signaling pathways play an important role in IL-22-mediated increases in inflammatory mediators. Microarray analyses revealed upregulated expression of inflammation-related genes in IL-22-treated HT22 cells. Finally, we found that IL-22Ralpha is spontaneously expressed in the brain and is upregulated in inflamed mouse brain. Overall, our results demonstrate that interaction of IL-22 with IL-22Ralpha plays a role in the development of inflammatory responses in the brain. |
