抗分泌因子可抑制肠道炎症和分泌过多。
Antisecretory factor suppresses intestinal inflammation and hypersecretion.
作者信息
Johansson E, Jennische E, Lange S, Lönnroth I
机构信息
Department of Medical Microbiology and Immunology, University of Gothenburg, Sweden.
出版信息
Gut. 1997 Nov;41(5):642-5. doi: 10.1136/gut.41.5.642.
BACKGROUND
Antisecretory factor (AF) is a recently identified regulatory protein which inhibits the intestinal fluid secretion induced by cholera toxin.
AIMS
To test the effect of AF on: (a) inflammation and hypersecretion induced by toxin A from Clostridium difficile; and (b) morphological changes and hypersecretion induced by okadaic acid (the blue mussel toxin) in rat intestinal mucosa.
METHODS
Morphological changes and fluid accumulation were observed in intestinal loops challenged with 1 microgram of toxin A or 3 micrograms of okadaic acid administered before or after injection of 0.1 microgram of recombinant AF (rAF).
RESULTS
The cytotoxic and inflammatory reaction caused by toxin A was abolished after treatment with rAF given either intraveneously or intraluminally prior to the toxin or one hour after the toxin. The intestinal fluid response induced by toxin A and okadaic acid was reduced 55-80% by rAF. However, the characteristic increase in goblet cells at the tips of villi in the okadaic acid treated mucosa was not inhibited by rAF.
CONCLUSION
Results suggest that AF might be involved in protection against inflammation and in counteracting dehydration caused by enterotoxins. Both effects are probably mediated via the enteric nervous system.
背景
抗分泌因子（AF）是一种最近发现的调节蛋白，可抑制霍乱毒素诱导的肠液分泌。
目的
测试AF对以下方面的作用：（a）艰难梭菌毒素A诱导的炎症和分泌亢进；（b）冈田酸（蓝贻贝毒素）在大鼠肠黏膜中诱导的形态学变化和分泌亢进。
方法
在用0.1微克重组AF（rAF）注射之前或之后，观察用1微克毒素A或3微克冈田酸攻击的肠袢中的形态学变化和液体蓄积。
结果
在用毒素之前静脉内或腔内给予rAF或在毒素作用后1小时给予rAF后，毒素A引起的细胞毒性和炎症反应被消除。rAF使毒素A和冈田酸诱导的肠液反应降低了55%至80%。然而，rAF并未抑制冈田酸处理的黏膜中绒毛尖端杯状细胞的特征性增加。
结论
结果表明，AF可能参与对抗炎症和抵消肠毒素引起的脱水。这两种作用可能都是通过肠神经系统介导的。
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