Imaeda H, Miura S, Serizawa H, Toda K, Ohkubo N, Kimura H, Yoshioka M, Tsuchiya M, Tso P
Department of Medicine, School of Medicine, Keio University, Tokyo, Japan.
Immunol Lett. 1993 Nov;38(3):253-8. doi: 10.1016/0165-2478(93)90014-s.
Effects of absorption of long and middle chain fatty acids on IgA secretion into the intestinal lumen and intestinal lymph and the factors which evoke changes in IgA secretion during the absorptive process were examined in rat small intestine. Bidirectional secretion of IgA from the intestinal mucosa into the intestinal lumen and intestinal lymph was continuously observed in the control condition. Perfusion of oleic acid (a long-chain fatty acid) micelle into the jejunal loop induced a significant increase in IgA output into the intestinal lymph. In contrast, lymphatic output of IgA was significantly decreased when oleic acid micelle was administered intraduodenally. Absorption of octanoic acid, a middle-chain fatty acid, did not produce any significant changes in IgA output into either direction. CR1505, a CCK-receptor antagonist, significantly attenuated the oleic acid-induced increase in IgA secretion into the intestinal lumen, but did not affect the oleic acid-induced decrease in lymphatic IgA secretion. Pluronic L-81, an inhibitor of chylomicron formation and secretion, significantly attenuated the decrease in IgA output into the intestinal lymph during oleic acid absorption without affecting the luminal IgA output. The rate of release of IgA into the intestinal lumen is stimulated by absorption of long-chain fatty acids possibly through the influence of locally released CCK, while the transport process of IgA into lymphatics is controlled by a different mechanism which is closely correlated with the intracellular formation and secretion of chylomicron.
在大鼠小肠中研究了长链和中链脂肪酸吸收对IgA分泌到肠腔和肠淋巴中的影响，以及在吸收过程中引起IgA分泌变化的因素。在对照条件下持续观察到IgA从肠黏膜向肠腔和肠淋巴的双向分泌。将油酸（一种长链脂肪酸）微团灌注到空肠肠袢中可导致IgA向肠淋巴的输出显著增加。相反，当十二指肠内给予油酸微团时，IgA的淋巴输出显著减少。中链脂肪酸辛酸的吸收对IgA向任一方向的输出均未产生任何显著变化。CCK受体拮抗剂CR1505显著减弱了油酸诱导的IgA向肠腔分泌的增加，但不影响油酸诱导的淋巴IgA分泌的减少。普朗尼克L-81，一种乳糜微粒形成和分泌的抑制剂，显著减弱了油酸吸收期间IgA向肠淋巴输出的减少，而不影响肠腔IgA输出。长链脂肪酸的吸收可能通过局部释放的CCK的影响刺激IgA向肠腔的释放速率，而IgA向淋巴管的转运过程受一种不同的机制控制，该机制与乳糜微粒的细胞内形成和分泌密切相关。
