Crowe S E, Soda K, Stanisz A M, Perdue M H
Intestinal Disease Research Unit, McMaster University, Hamilton, Ontario, Canada.
Am J Physiol. 1993 Apr;264(4 Pt 1):G617-23. doi: 10.1152/ajpgi.1993.264.4.G617.
In vivo uptake of the probe 51Cr-labeled EDTA from the jejunum of egg albumin (EA)-sensitized rats was compared with controls at baseline and after intraluminal antigen challenge. Probe recovery in blood was 60-80% greater in sensitized animals during the baseline period, suggesting that sensitization resulted in increased intestinal permeability. Sensitized, but not control, rats demonstrated a 15-fold increase in 51Cr-EDTA uptake after intraluminal antigen; no change occurred with an unrelated protein. Macromolecular recovery was also enhanced in sensitized animals, since serum levels of immunoreactive EA were elevated 14-fold compared with controls. Antigen challenge was accompanied by biochemical (protease release) and morphological (reduced numbers) evidence of mast cell degranulation in sensitized rats. The neurotoxin tetrodotoxin (applied directly to ligated jejunal segments) inhibited EA-induced uptake of 51Cr-EDTA and antigen. In isolated jejunum from sensitized rats, tetrodotoxin reduced secretory responses to luminal, but not serosal, antigen. These results indicate that neural factors may influence the uptake of molecules from the gut lumen during intestinal anaphylaxis.
在基线期以及腔内抗原激发后,将51Cr标记的乙二胺四乙酸(EDTA)探针在卵清蛋白(EA)致敏大鼠空肠中的体内摄取情况与对照组进行了比较。在基线期,致敏动物血液中的探针回收率比对照组高60 - 80%,这表明致敏导致肠道通透性增加。致敏大鼠在腔内抗原激发后,51Cr - EDTA摄取量增加了15倍,而对照组大鼠无变化;用无关蛋白质激发则无改变。致敏动物的大分子回收率也有所提高,因为与对照组相比,血清中免疫反应性EA水平升高了14倍。抗原激发伴随着致敏大鼠肥大细胞脱颗粒的生化证据(蛋白酶释放)和形态学证据(数量减少)。神经毒素河豚毒素(直接应用于结扎的空肠段)抑制了EA诱导的51Cr - EDTA摄取和抗原摄取。在致敏大鼠的离体空肠中,河豚毒素降低了对腔内抗原而非浆膜抗原的分泌反应。这些结果表明,在肠道过敏反应期间,神经因素可能影响肠道腔内分子的摄取。