Soda K, Kawabori S, Kanai N, Bienenstock J, Perdue M H
Department of Pathology, McMaster University, Hamilton, Ont., Canada.
Int Arch Allergy Immunol. 1993;101(1):39-46. doi: 10.1159/000236496.
In conventional rats, we have previously demonstrated that corticosteroid treatment caused macrophage engulfment and destruction of intestinal mucosal mast cells and eosinophils by 24 h without evidence of local tissue destruction, inflammation or secretion of rat mast cell protease II. As the growth and survival of these cells appear to be dependent on factors derived from T lymphocytes, we examined the response in congenitally athymic rnu/rnu rats and euthymic rnu/+ rats 35 days after parasitic infection. Rats were injected intraperitoneally with 1 mg dexamethasone and sections of jejunum were examined at 0, 7, 13 and 24 h. The numbers of mucosal mast cells significantly decreased in both groups and became less than 30% of the original values at 24 h. Tissue mast cell protease decreased similarly. However, protease in serum did not increase and there were no inflammatory changes at any time. The numbers of eosinophils also rapidly decreased and became less than 20% at 24 h in both rnu/rnu and rnu/+ rats. By electron microscopy, we saw granular changes (fusion) in mast cells and nuclear changes (apoptosis) in eosinophils by 7 h after corticosteroid in athymic rats. Macrophage engulfment of these cells was observed at 7 and 13 h. Our results suggest that inflammatory cell depletion by macrophages is not dependent on suppression of typical thymus-derived T lymphocytes, and may be due either to direct effects of steroids on the cells themselves, or indirectly upon cells other than T cells which normally supply maintenance and growth factors for them.
在传统大鼠中，我们之前已经证明，皮质类固醇治疗在24小时内可导致巨噬细胞吞噬并破坏肠道黏膜肥大细胞和嗜酸性粒细胞，且没有局部组织破坏、炎症或大鼠肥大细胞蛋白酶II分泌的证据。由于这些细胞的生长和存活似乎依赖于T淋巴细胞衍生的因子，我们在寄生虫感染35天后检查了先天性无胸腺的rnu/rnu大鼠和有胸腺的rnu/+大鼠的反应。大鼠腹腔注射1毫克地塞米松，并在0、7、13和24小时检查空肠切片。两组黏膜肥大细胞数量均显著减少，在24小时时降至原始值的30%以下。组织肥大细胞蛋白酶也有类似下降。然而，血清中的蛋白酶没有增加，且在任何时候都没有炎症变化。嗜酸性粒细胞数量也迅速减少，在24小时时，rnu/rnu和rnu/+大鼠中的嗜酸性粒细胞数量均降至20%以下。通过电子显微镜观察，在无胸腺大鼠中，皮质类固醇处理7小时后，我们在肥大细胞中看到颗粒变化（融合），在嗜酸性粒细胞中看到核变化（凋亡）。在7和13小时观察到巨噬细胞对这些细胞的吞噬。我们的结果表明，巨噬细胞导致的炎症细胞耗竭不依赖于典型胸腺来源的T淋巴细胞的抑制，可能是由于类固醇对细胞本身的直接作用，或间接作用于通常为它们提供维持和生长因子的T细胞以外的细胞。
