Luettig J, Rosenthal R, Barmeyer C, Schulzke J D
Institute of Clinical Physiology; Department of Gastroenterology; Charité ; Berlin, Germany.
Tissue Barriers. 2015 Apr 3;3(1-2):e977176. doi: 10.4161/21688370.2014.977176. eCollection 2015.
The epithelial tight junction determines the paracellular water and ion movement in the intestine and also prevents uptake of larger molecules, including antigens, in an uncontrolled manner. Claudin-2, one of the 27 mammalian claudins regulating that barrier function, forms a paracellular channel for small cations and water. It is typically expressed in leaky epithelia like proximal nephron and small intestine and provides a major pathway for the paracellular transport of sodium, potassium, and fluid. In intestinal inflammation (Crohn's disease, ulcerative colitis), immune-mediated diseases (celiac disease), and infections (HIV enteropathy), claudin-2 is upregulated in small and large intestine and contributes to diarrhea via a leak flux mechanism. In parallel to that upregulation, other epithelial and tight junctional features are altered and the luminal uptake of antigenic macromolecules is enhanced, for which claudin-2 may be partially responsible through induction of tight junction strand discontinuities.
上皮紧密连接决定了肠道中细胞旁的水和离子移动，还能防止包括抗原在内的大分子以不受控制的方式被吸收。Claudin-2是调节该屏障功能的27种哺乳动物Claudin蛋白之一，它形成了一个允许小阳离子和水通过的细胞旁通道。它通常在如近端肾小管和小肠等渗漏上皮中表达，并为钠、钾和液体的细胞旁转运提供主要途径。在肠道炎症（克罗恩病、溃疡性结肠炎）、免疫介导疾病（乳糜泻）和感染（HIV肠病）中，Claudin-2在小肠和大肠中上调，并通过渗漏通量机制导致腹泻。与这种上调同时发生的是，其他上皮和紧密连接特征发生改变，抗原性大分子的腔内摄取增加，Claudin-2可能通过诱导紧密连接链的间断对此负有部分责任。
