King S J, Miller H R, Newlands G F, Woodbury R G
Proc Natl Acad Sci U S A. 1985 Feb;82(4):1214-8. doi: 10.1073/pnas.82.4.1214.
Rats primed by infection with the intestinal nematode Nippostrongylus brasiliensis and challenged intravenously with soluble whole-worm antigen undergo systemic anaphylactic shock. The primary lesions are in the gut and include increased permeability of the mucosa together with release, into enteric secretions, of a mucosal mast cell (MMC)-specific serine proteinase, rat mast cell protease II (RMCP-II). This enzyme is also released into the blood of shocked rats. These manifestations of anaphylaxis were abolished in rats previously treated with corticosteroids (methylprednisolone acetate, 25 mg per kg of body weight, 48 and 24 hr before i.v. challenge with antigen). Suppression of the response was associated with depletion of RMCP-II and of MMC from the intestinal mucosa. Depletion occurred 4-24 hr after treatment with as little as 1 mg of methylprednisolone per kg. By contrast, neither connective tissue mast cells nor serum levels of parasite-specific IgE were depleted in rats given 2 X 25 mg of methylprednisolone per kg. The capacity of unprimed treated rats to mount passive cutaneous anaphylaxis was, however, impaired.
经巴西日圆线虫肠道线虫感染致敏的大鼠，静脉注射可溶性全虫抗原后会发生全身性过敏性休克。主要病变发生在肠道，包括粘膜通透性增加，以及一种粘膜肥大细胞（MMC）特异性丝氨酸蛋白酶——大鼠肥大细胞蛋白酶II（RMCP-II）释放到肠分泌物中。这种酶也会释放到休克大鼠的血液中。在用皮质类固醇（醋酸甲泼尼龙，每公斤体重25毫克，在静脉注射抗原前48小时和24小时）预先处理的大鼠中，这些过敏反应表现被消除。反应的抑制与RMCP-II和MMC从肠粘膜中耗竭有关。在每公斤仅用1毫克甲泼尼龙治疗后4至24小时发生耗竭。相比之下，每公斤给予2×25毫克甲泼尼龙的大鼠中，结缔组织肥大细胞和寄生虫特异性IgE的血清水平均未耗竭。然而，未致敏的经处理大鼠引发被动皮肤过敏反应的能力受损。
