Reglero-Real Natalia, García-Weber Diego, Millán Jaime
Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Campus Cantoblanco, 28049 Madrid, Spain; William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Campus Cantoblanco, 28049 Madrid, Spain.
Mediators Inflamm. 2016;2016:7650260. doi: 10.1155/2016/7650260. Epub 2016 Jan 28.
During the inflammatory response, immune cells egress from the circulation and follow a chemotactic and haptotactic gradient within the tissue, interacting with matrix components in the stroma and with parenchymal cells, which guide them towards the sites of inflammation. Polarized epithelial cells compartmentalize tissue cavities and are often exposed to inflammatory challenges such as toxics or infections in non-lymphoid tissues. Apicobasal polarity is critical to the specialized functions of these epithelia. Indeed, a common feature of epithelial dysfunction is the loss of polarity. Here we review evidence showing that apicobasal polarity regulates the inflammatory response: various polarized epithelia asymmetrically secrete chemotactic mediators and polarize adhesion receptors that dictate the route of leukocyte migration within the parenchyma. We also discuss recent findings showing that the loss of apicobasal polarity increases leukocyte adhesion to epithelial cells and the consequences that this could have for the inflammatory response towards damaged, infected or transformed epithelial cells.
在炎症反应过程中,免疫细胞从循环系统中逸出,并沿着组织内的趋化和趋触梯度移动,与基质中的基质成分以及实质细胞相互作用,这些成分和细胞引导它们前往炎症部位。极化的上皮细胞分隔组织腔,并且在非淋巴组织中经常面临诸如毒素或感染等炎症挑战。顶基极性对于这些上皮细胞的特殊功能至关重要。实际上,上皮功能障碍的一个共同特征是极性丧失。在这里,我们综述了表明顶基极性调节炎症反应的证据:各种极化上皮细胞不对称地分泌趋化介质并使粘附受体极化,这些受体决定了白细胞在实质内的迁移途径。我们还讨论了最近的研究结果,这些结果表明顶基极性的丧失会增加白细胞与上皮细胞的粘附,以及这可能对针对受损、感染或转化的上皮细胞的炎症反应产生的后果。