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免疫球蛋白G与免疫球蛋白E:抗原诱导豚鼠气管收缩的介质

IgG vs IgE: mediators of antigen-induced guinea pig tracheal contraction.

作者信息

Regal J F

出版信息

Immunopharmacology. 1984 Dec;8(3-4):111-9. doi: 10.1016/0162-3109(84)90014-6.

Abstract

Guinea pig IgG and IgE were employed in these studies to determine whether different mediators were responsible for IgG- and IgE-mediated contraction of guinea pig trachea. Isolated tracheal strips were passively sensitized using IgG- or IgE-type antibody to ovalbumin which had been separated using Protein A Sepharose. The antigen-induced contraction of tracheae sensitized with either IgG or IgE was delayed by diphenhydramine (10(-5) M) and significantly enhanced by aspirin (1.1 X 10(-4) M). The leukotriene antagonist FPL 55712 (1.9 X 10(-5) M) decreased the duration of the IgG-mediated contraction but not that of the IgE-mediated contraction. Diphenhydramine in combination with FPL 55712 caused a greater inhibition of the IgG-mediated tracheal contraction than either antagonist alone. In contrast, the IgE-mediated response was inhibited to the same extent by a combination of FPL 55712 and diphenhydramine as with diphenhydramine alone. The lipoxygenase inhibitor nordihydroguaiaretic acid in combination with diphenhydramine inhibited the antigen-induced contraction to a greater extent than diphenhydramine alone in the IgG, but not in the IgE-sensitized trachea. Leukotriene release from trachea was assessed by contraction of the longitudinal muscle of an unsensitized guinea pig ileum mounted in the same tissue bath. On ovalbumin challenge, leukotriene release was detected from IgG-sensitized trachea but only minimally from IgE-sensitized trachea. Histamine release was detectable on antigen challenge of IgG- and IgE-sensitized trachea. Heating IgG (56 degrees C for 4 h) did not alter its ability to mediate histamine or leukotriene release.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在这些研究中使用豚鼠IgG和IgE,以确定是否不同的介质负责IgG和IgE介导的豚鼠气管收缩。使用已用蛋白A琼脂糖分离的抗卵清蛋白IgG或IgE型抗体对分离的气管条进行被动致敏。用苯海拉明(10^(-5)M)可延迟IgG或IgE致敏的气管对抗原诱导的收缩,而阿司匹林(1.1×10^(-4)M)可显著增强该收缩。白三烯拮抗剂FPL 55712(1.9×10^(-5)M)可缩短IgG介导的收缩持续时间,但对IgE介导的收缩持续时间无影响。苯海拉明与FPL 55712联合使用对IgG介导的气管收缩的抑制作用比单独使用任何一种拮抗剂都更大。相反,FPL 55712和苯海拉明联合使用对IgE介导的反应的抑制程度与单独使用苯海拉明时相同。脂氧合酶抑制剂去甲二氢愈创木酸与苯海拉明联合使用时,在IgG致敏的气管中比单独使用苯海拉明更能抑制抗原诱导的收缩,但在IgE致敏的气管中则不然。通过安装在同一组织浴中的未致敏豚鼠回肠纵肌的收缩来评估气管中白三烯的释放。在卵清蛋白激发时,可从IgG致敏的气管中检测到白三烯释放,但从IgE致敏的气管中仅检测到极少释放。在IgG和IgE致敏的气管进行抗原激发时可检测到组胺释放。加热IgG(56℃,4小时)不会改变其介导组胺或白三烯释放的能力。(摘要截断于250字)

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