| First Author | Wang D | Year | 2017 |
| Journal | Inflammation | Volume | 40 |
| Issue | 4 | Pages | 1191-1203 |
| PubMed ID | 28466432 | Mgi Jnum | J:310795 |
| Mgi Id | MGI:6511448 | Doi | 10.1007/s10753-017-0562-0 |
| Citation | Wang D, et al. (2017) Macrophage Subset Expressing CD169 in Peritoneal Cavity-Regulated Mucosal Inflammation Together with Lower Levels of CCL22. Inflammation 40(4):1191-1203 |
| abstractText | Crohn's disease (CD) and ulcerative colitis (UC) are the most widely known types of inflammatory bowel diseases (IBD) and have been paid more attention due to their increasing incidence and a substantial increase in the risk of colorectal cancer (CRC). However, the phenotype and, more importantly, the function in the regulation of mucosal inflammation by different macrophages are poorly understood, even though macrophages constitute a major subset of intestinal myeloid cells. The results firstly showed that the subset of peritoneal CD11b(+)CD169(+) macrophages increased and CCL22 expression level decreased significantly during the DSS-induced colitis. DSS-induced colitis was alleviated in CD169-DTR mice at least partially due to the deletion CD169(+) macrophages. Moreover, the CCL22 expression level in peritoneal macrophages from CD169-DTR mice was much higher than that from WT mice with DSS-induced colitis. And, the cell-sorting result revealed that CD11b(+)CD169(+) macrophage cells did not express CCL22 dominantly. Further experiment in vivo demonstrated that treatment with recombinant murine CCL22 (rmCCL22) ameliorated the clinical symptoms of DSS-induced colitis. All these data indicated that macrophage subset of CD11b(+)CD169(+) from peritoneal cavity played critical role probably together with low levels of CCL22 in DSS-induced colitis. |
