| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Outline of Final Research Achievements |
In the present study, we investigated the role of CD206 positive intestinal macrophages in the mucosal repair after inflammation. We used transgenic mice expressing human diphtheria toxin (DT) receptor under the control of CD206 gene promoter. A part of the resident intestinal macrophages expressed CD206, and about 90% of this population was depleted after DT injection. In the experimental colitis model, the recovery of body weight loss and improvement of disease activity index was significantly delayed in CD206-depleted mice compared with WT mice. The resident intestinal macrophages promoted the wound repair of colonic epithelial cells after the injury. We found that the intestinal macrophages from CD206-depleted mice did not affect the wound repair of colonic epithelial cells after the injury.
The present findings suggest that CD206 positive intestinal macrophages play an important role in the intestinal mucosal repair following inflammatory damage such as inflammatory bowel disease.
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