CCL25-CCR9 Interactions Regulate the Function of iNKT Cells in Oxazolone-Induced Colitis in MiceReport as inadecuate




CCL25-CCR9 Interactions Regulate the Function of iNKT Cells in Oxazolone-Induced Colitis in Mice - Download this document for free, or read online. Document in PDF available to download.

Background

Natural killer T NKT cells share phenotypic and functional properties with both conventional natural killer cells and T cells. These cells might have an important role in the pathogenesis of ulcerative colitis UC. The interaction of chemokine ligand 25 CCL25 with chemokine receptor 9 CCR9 is involved in gut-specific migration of leukocytes and induces regulatory T cells Tregs to migrate to the intestine in chronic ileitis.

Methodology-Findings

In UC patients, NKT receptor CD161, CCL25, and CCR9 expression levels were evaluated by qRT-PCR. A murine model of oxazolone-induced colitis was induced in BALB-c mice. The mRNA levels of NK1.1, CCL25 and CCR9, and pro-inflammatory cytokines in mice were evaluated. The CCR9 expression on Type I or invariant NKT iNKT cells, and the iNKT cells chemotaxis are observed according to flow cytometry. NKT receptor CD161, CCL25 and CCR9 expression levels were significantly increased in UC patients. And, the mRNA expression levels of NK1.1, CCL25 and CCR9 were increased in oxazolone-induced colitis in mice. The production of pro-inflammatory cytokines was significantly increased, especially interleukin 4 IL-4, IL-10 and IL-13. We observed significantly increased CCR9 expression on iNKT cells. Furthermore, we found an increased iNKT population and enhanced chemotaxis during oxazolone-induced colitis.

Conclusions-Significance

Our study suggests that CCL25-CCR9 interactions may promote the induction and function of iNKT cells during oxazolone-induced colitis. These findings may have important implications for UC treatment and suggest a role for CCR9 inhibitors.



Author: Siying Zhu , Yuntao Bing , Xiaobing Wang, Qiao Yu, Yipeng Wang, Shufang Xu, Lu Song, Xintao Wang, Bing Xia, Youqing Zhu , Rui Zho

Source: http://plos.srce.hr/



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