Theodorou V, Fioramonti J, Junien J L, Bueno L
Department of Pharmacology, Institut National de la Recherche Agronomique, Toulouse, France.
Aliment Pharmacol Ther. 1994 Jun;8(3):301-7. doi: 10.1111/j.1365-2036.1994.tb00292.x.
The effect of beta-lactoglobulin (beta-LGI) challenge on net water movements into the proximal colon and the role of Interleukin-1 (IL-1), prostaglandins and mast cell degranulation on the challenge-induced net water changes were assessed in vivo using isolated colonic loops in anaesthetized guinea-pigs immunized to bovine milk.
beta-lactoglobulin challenge infused into the colonic loop during 30 min reversed the net water flux into a net secretion during the period of antigen infusion. Doxantrazole, a mast cell stabilizing agent, administered 120 min before challenge infusion, suppressed challenge-induced hypersecretion. Similarly recombinant IL-1 receptor antagonist protein abolished the antigen-induced colonic secretory effect. Indomethacin, a prostaglandin synthesis inhibitor, administered 20 min prior to antigen infusion, significantly (P < 0.05) reduced, but did not abolish, the challenge-induced colonic secretory effect.
These results suggest that IL-1 plays an important role in antigen challenge-induced colonic hypersecretion which involves mast cell degranulation and prostaglandin release.
利用在麻醉状态下对牛乳免疫的豚鼠的离体结肠肠袢，在体内评估β-乳球蛋白（β-LGI）激发对近端结肠净水分移动的影响，以及白细胞介素-1（IL-1）、前列腺素和肥大细胞脱颗粒在激发诱导的净水分变化中的作用。
在30分钟内将β-乳球蛋白激发液注入结肠肠袢，在抗原注入期间使净水分通量逆转成净分泌。在激发注入前120分钟给予肥大细胞稳定剂多克替拉佐，可抑制激发诱导的分泌亢进。同样，重组IL-1受体拮抗剂蛋白消除了抗原诱导的结肠分泌效应。在抗原注入前20分钟给予前列腺素合成抑制剂吲哚美辛，可显著（P<0.05）降低但未消除激发诱导的结肠分泌效应。
这些结果表明，IL-1在抗原激发诱导的结肠分泌亢进中起重要作用，这涉及肥大细胞脱颗粒和前列腺素释放。
