INTESTINAL ANAPHYLAXIS - RADIATION-INDUCED SUPPRESSION
INTESTINAL ANAPHYLAXIS - RADIATION-INDUCED SUPPRESSION
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DOI：
10.1152/ajpgi.1994.267.4.g709
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发表时间：
1994-10-01
影响因子：
4.5
通讯作者：
CASTRO, G
中科院分区：
文献类型：
--
作者：
HARARI, Y;KESTER, D;CASTRO, G
胃肠道对电离辐射非常敏感。该系统中对辐射最敏感的细胞是肥大细胞和上皮细胞。这篇文章描述了实验测试假设，即辐射抑制粘膜免疫反应，其中肥大细胞和上皮参与。通过观察电离辐射对旋毛虫感染致敏大鼠空肠过敏介导的Cl-分泌的影响，验证了这一假设。体外电生理检测抗原诱导的Cl-分泌。大鼠接种3 × 10(3)螺旋体幼虫免疫，30-50天后，暴露于钴-60 γ源的腹部全照射下。剂量分别为5、7和9 Gy。在放疗后1、3、5、7、14和21天，评估空肠段的免疫反应性。（对抗原攻击的抑制时间与辐射剂量直接相关。）5gy辐照后的抗原性反应恢复为5dpi。7 Gy时，反应性在1 ~ 5 DPI范围内完全抑制，在5 ~ 14 DPI范围内部分表达，在21 DPI范围内完全恢复。9 Gy的剂量在21天内完全抑制了免疫反应。在1-5 DPI时，空肠对外源性Cl-分泌剂的完全反应表明，辐射的免疫抑制作用不是由于上皮水平分泌过程的破坏。被动皮肤过敏反应测定的血清免疫球蛋白E水平在辐照动物和未辐照动物中相似，表明对抗原挑战的反应失败不是由于同细胞性抗体功能障碍的变化。对该系统的进一步检查表明，在大鼠暴露于辐射后，肥大细胞被破坏。阿利新蓝染色未检出粘膜肥大细胞，黏膜组胺水平降低90% 1-5 DPI。没有染色和组胺水平降低也与大鼠肥大细胞蛋白酶II的低组织水平有关。由于肥大细胞是过敏反应介导的Cl-分泌的必需细胞，因此肥大细胞的缺失可以解释受辐射大鼠空肠对抗原刺激反应的失败。另一方面，在没有粘膜肥大细胞的情况下，随后对抗原的反应性恢复。对这一现象的一种可能解释是，粘膜肥大细胞的功能由另一种细胞类型承担时发生了适应。
The gastrointestinal tract is highly sensitive to ionizing radiation. Some of the most radiosensitive cells in this system are mast cells and epithelium. This article describes experiments that test the hypothesis that irradiation suppresses mucosal immune responses in which mast cells and epithelium are involved. The hypothesis was tested by examining the impact of ionizing radiation on anaphylactically mediated Cl- secretion in jejunum of rats sensitized by Trichinella spiralis infection and challenged with antigen derived from the parasite. Antigen-induced Cl- secretion was measured electrophysiologically in vitro. Rats were immunized by inoculation with 3 x 10(3) T. spiralis larvae and, 30-50 days later, exposed to total abdominal irradiation from a cobalt-60 gamma source. Doses were 5, 7, and 9 Gy. At 1, 3, 5, 7, 14, and 21 days postirradiation (DPI), jejunal segments were assessed for immune responsiveness. (Duration of suppression to antigenic challenge was directly related to radiation dose.) Recovery of response to antigenic challenge after irradiation with 5 Gy was complete by 5 DPI. At 7 Gy, responsiveness was totally suppressed from I to 5 DPI, was partially expressed from 5 to 14 DPI, and was completely restored by 21 DPI. A dose of 9 Gy completely suppressed immune responsiveness throughout the 21-day period. Full responsiveness of jejunum to exogenous Cl- secretagogues at 1-5 DPI indicates that the immunosuppressive effect of radiation was not due to a breakdown in the secretory process at the epithelium level. Serum immunoglobulin E levels, as determined by passive cutaneous anaphylaxis, were similar in irradiated and nonirradiated animals, indicating that failure to respond to antigenic challenge was not due to changes in the malfunctioning of homocytotropic antibody. Further examination of the system revealed that mast cells were destroyed after exposure of rats to radiation. Mucosal mast cells were undetectable by Alcian blue staining, and the level of mucosal histamine was reduced by 90% 1-5 DPI. Absence of staining and reduced histamine levels were also associated with low tissue levels of rat mast cell protease II. Because mast cells are necessary for expression of anaphylactically mediated Cl- secretion, their absence could explain the failure of jejunum from irradiated rats to respond to antigenic stimulation. On the other hand, subsequent recovery of responsiveness to antigen occurred in the absence of mucosal mast cells. A possible explanation of this phenomenon is that an adaptation occurs in which the function of the mucosal mast cell is assumed by another cell type.