Cummins A G, Kenny A L, Duncombe V M, Bolin T D, Davis A E
Gastrointestinal Unit, University of N.S.W., Australia.
Immunol Cell Biol. 1987 Aug;65 ( Pt 4):357-63. doi: 10.1038/icb.1987.40.
Serum rat mucosal mast cell protease II (RMCPII) was measured in protein-deficient rats to assess mucosal mast cell (MMC) activation during primary infection with the nematode, Nippostrongylus brasiliensis, and during systemic anaphylaxis produced by Nippostrongylus antigen in immune animals. In the first study, serum RMCPII increased 4-fold by day 15 after infection. By day 20, serum RMCPII continued to rise in protein-deficient animals, but decreased in nutritionally normal animals. This was associated with impaired worm rejection in protein-deficient rats. During systemic anaphylaxis, serum RMCPII was elevated in three groups of protein-deficient rats on 6%, 8% and 10% low protein diets and in nutritionally normal rats. All protein-deficient rats exhibited 3 to 7-fold less mucosal permeability of the small intestine to Evan's blue dye injected intravenously compared to nutritionally normal animals following anaphylactic stimulation. These results demonstrated that MMC are activated during infection in protein deficiency, and suggest that reduced MMC function does not explain delay in worm expulsion. Impaired mucosal anaphylaxis in protein deficiency could not be attributed to a failure of MMC response.
在蛋白质缺乏的大鼠中检测血清大鼠黏膜肥大细胞蛋白酶II（RMCPII），以评估在感染巴西日圆线虫的初次感染期间以及在免疫动物中由日圆线虫抗原引发的全身过敏反应期间黏膜肥大细胞（MMC）的激活情况。在第一项研究中，感染后第15天血清RMCPII增加了4倍。到第20天，蛋白质缺乏动物的血清RMCPII持续上升，而营养正常的动物则下降。这与蛋白质缺乏大鼠中蠕虫排斥受损有关。在全身过敏反应期间，三组分别食用6%、8%和10%低蛋白饮食的蛋白质缺乏大鼠以及营养正常的大鼠的血清RMCPII均升高。与过敏刺激后营养正常的动物相比，所有蛋白质缺乏大鼠的小肠对静脉注射伊文思蓝染料的黏膜通透性均降低3至7倍。这些结果表明，在蛋白质缺乏的感染过程中MMC被激活，并且提示MMC功能降低并不能解释蠕虫排出延迟的现象。蛋白质缺乏时黏膜过敏反应受损不能归因于MMC反应的失败。
