Intestinal epithelial hyperpermeability: update on the pathogenesis of gut mucosal barrier dysfunction in critical illness.
Intestinal epithelial hyperpermeability: update on the pathogenesis of gut mucosal barrier dysfunction in critical illness.
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DOI：
10.1097/00075198-200304000-00011
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发表时间：
2003-04-01
影响因子：
3.3
通讯作者：
Fink, Mitchell P
中科院分区：
文献类型：
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作者：
Fink, Mitchell P
审查目的：相邻上皮细胞之间的紧密连接对于维持各种器官（如肝、肺、肾和肠）中组成不同的流体隔室是必不可少的。这些上皮器官通常在称为多器官功能障碍综合征的病症中受到影响，这可能使患有脓毒症或与控制不良的全身性炎症相关的其他病症的患者的临床病程复杂化。肠道是解决这一问题的有效模型，使用还原论体外模型的研究和使用实验室动物进行的实验开始阐明导致危重病继发肠上皮细胞通透性过高的细胞和生化机制。已经确定的一个关键因素是一氧化氮和相关物质的过量产生，尽管其他因素，例如细胞因子白细胞介素6的表达增加，似乎也很重要。一个新的描述，类胡萝卜素分子，高流动性组B1，增加体外培养的上皮细胞单层和小鼠回肠mucosa in vivo.SUMMARY：上皮细胞功能障碍可能是一个共同的最终途径，有助于器官功能障碍败血症和其他形式的危重病。
PURPOSE OF REVIEW: Tight junctions between adjacent epithelial cells are essential for the maintenance of compositionally distinct fluid compartments in various organs, such as the liver, lungs, kidneys, and intestine. These epithelial organs are commonly affected in the condition known as multiple organ dysfunction syndrome, which can complicate the clinical course of patients with sepsis or other conditions associated with poorly controlled systemic inflammation. The gut serves as a useful model for this problem, and studies using reductionist in vitro models and experiments carried out using laboratory animals are starting to clarify the cellular and biochemical mechanisms that are responsible for intestinal epithelial hyperpermeability secondary to critical illness.RECENT FINDINGS: One key factor that has been identified is excessive production of nitric oxide and related species, although other factors, such as increased expression of the cytokine interleukin 6, appear to be important as well. A newly described, cytokine-like molecule, high-mobility group B1, increases permeability of cultured epithelial monolayers in vitro and murine ileal mucosa in vivo.SUMMARY: Epithelial dysfunction may be a common final pathway contributing to organ dysfunction in sepsis and other forms of critical illness.