Pathophysiological role of mast cells on the bone homeostasis.

在胶原诱导的关节炎小鼠的炎症足爪中，肥大细胞的数量显著增加，并且肥大细胞是产生TNF-α的主要细胞之一。TNF-α阳性肥大细胞广泛存在于关节炎小鼠的整个炎症滑膜中，并且一些肥大细胞在显着的骨和软骨破坏区域中与破骨细胞紧密接近。用肥大细胞膜稳定剂治疗8周和糜蛋白酶抑制剂治疗4周显著降低了胶原诱导的关节炎的临床和X射线评分，并降低了关节炎小鼠发炎爪中TNF-α阳性肥大细胞的数量和TNF-α的mRNA水平。肥大细胞膜稳定剂和糜酶抑制剂处理也减少破骨细胞的数量。提示肥大细胞可能参与骨代谢和胶原诱导性关节炎的发病机制。

The number of mast cells was markedly increased in the inflamed paws of collagen-induced arthritis in mice, and mast cells were one of the major cells producing TNF-alpha. TNF-alpha positive mast cells were present extensively throughout the inflamed synovium of arthritic mice, and some of the mast cells were in close proximity of osteoclasts in the area of marked bone and cartilage destruction. Treatment with a mast cell membrane stabilizer for 8 weeks and chymase inhibitor for 4 weeks significantly reduced clinical and X-ray scores of collagen-induced arthritis, and decreased the number of TNF-alpha positive mast cells and the mRNA levels of TNF-alpha in the inflamed paws of arthritic mice. The number of osteoclasts was also decreased by treatment with a mast cell membrane stabilizer and chymase inhibitor. These observations suggest that mast cells may be involved in bone metabolism and pathogenesis of collagen-induced arthritis in mice.