Department of Anatomy, Saint Petersburg State Paediatric Medical University, S. Petersburg, Russia.
Department of Anatomy, Ivanovo State Medical Academy, Ivanovo, Russia.
Tissue Cell. 2021 Oct;72:101529. doi: 10.1016/j.tice.2021.101529. Epub 2021 Apr 20.
Although the general structure of the barrier between the gut and the blood is well known, many details are still missing. Here, we analyse the literature and our own data related to lipid transcytosis through adult mammalian enterocytes, and their absorption into lymph at the tissue level of the intestine. After starvation, the Golgi complex (GC) of enterocytes is in a resting state. The addition of lipids in the form of chyme leads to the initial appearance of pre-chylomicrons (ChMs) in the tubules of the smooth endoplasmic reticulum, which are attached at the basolateral plasma membrane, immediately below the 'belt' of the adhesive junctions. Then pre-ChMs move into the cisternae of the rough endoplasmic reticulum and then into the expansion of the perforated Golgi cisternae. Next, they pass through the GC, and are concentrated in the distensions of the perforated cisternae on the trans-side of the GC. The arrival of pre-ChMs at the GC leads to the transition of the GC to a state of active transport, with formation of intercisternal connections, attachment of cis-most and trans-most perforated cisternae to the medial Golgi cisternae, and disappearance of COPI vesicles. Post-Golgi carriers then deliver ChMs to the basolateral plasma membrane, fuse with it, and secret ChMs into the intercellular space between enterocytes at the level of their interdigitating contacts. Finally, ChMs are squeezed out into the interstitium through pores in the basal membrane, most likely due to the function of the actin-myosin 'cuff' around the interdigitating contacts. These pores appear to be formed by protrusions of the dendritic cells and the enterocytes per se. ChMs are absorbed from the interstitium into the lymphatic capillaries through the special oblique contacts between endothelial cells, which function as valves through the contraction-relaxation of bundles of smooth muscle cells in the interstitium. Lipid overloading of enterocytes results in accumulation of cytoplasmic lipid droplets, an increase in diameter of ChMs, inhibition of intra-Golgi transport, and fusion of ChMs in the interstitium. Here, we summarise and analyse recent findings, and discuss their functional implications.
尽管肠道和血液之间的屏障的一般结构已经广为人知，但仍有许多细节尚未被揭示。在这里，我们分析了与成年哺乳动物肠上皮细胞的脂类穿越以及它们在肠道组织水平被吸收进入淋巴相关的文献和我们自己的数据。在饥饿后，肠上皮细胞的高尔基体（GC）处于静止状态。食糜中脂质的加入导致前乳糜微粒（ChMs）首先出现在光滑内质网的小管中，这些小管附着在基底外侧质膜上，就在粘着连接的“带”下方。然后，前 ChMs 移动到粗面内质网的池，然后进入穿孔高尔基体池的扩张部。接下来，它们穿过 GC，并在 GC 的转位侧的穿孔池的扩张部中浓缩。前 ChMs 到达 GC 会导致 GC 过渡到活跃运输状态，形成内质网间连接，将最靠近 cis 和最靠近 trans 的穿孔内质网附着到中间高尔基体内质网，并使 COPI 囊泡消失。高尔基体后载体随后将 ChMs 递送至基底外侧质膜，与质膜融合，并将 ChMs 分泌到肠上皮细胞的相邻接触处的细胞间隙中。最后，ChMs 通过基底膜中的孔挤出到间质中，这很可能是由于相邻接触处的肌动球蛋白“袖口”的功能。这些孔似乎是由树突状细胞和肠上皮细胞本身的突起形成的。ChMs 通过内皮细胞之间的特殊斜向接触从间质中被吸收进入淋巴管，这些接触作为瓣膜，通过间质中平滑肌细胞束的收缩-松弛起作用。肠上皮细胞的脂质超负荷会导致细胞质脂质滴的积累、ChMs 直径的增加、内高尔基体运输的抑制以及 ChMs 在间质中的融合。在这里，我们总结和分析了最近的发现，并讨论了它们的功能意义。
