Department of Immunology, UConn Health School of Medicine, Farmington, CT 06030, USA.
Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Trends Mol Med. 2018 Mar;24(3):304-318. doi: 10.1016/j.molmed.2018.01.004. Epub 2018 Feb 9.
Organismal fitness demands proper response to neutralize the threat from infection or injury. At the mammalian intestinal epithelium barrier, the inflammasome coordinates an elaborate tissue repair response marked by the induction of antimicrobial peptides, wound-healing cytokines, and reparative proliferation of epithelial stem cells. The inflammasome in myeloid and intestinal epithelial compartments exerts these effects in part through maintenance of a healthy microbiota. Disease-associated mutations and elevated expression of certain inflammasome sensors have been identified. In many cases, inhibition of inflammasome activity has dramatic effects on disease outcome in mouse models of experimental colitis. Here, we discuss recent studies on the role of distinct inflammasome sensors in intestinal homeostasis and how this knowledge may be translated into a therapeutic setting.
生物体的适应性需要做出适当的反应来中和感染或损伤带来的威胁。在哺乳动物的肠道上皮屏障中,炎症小体协调了一个复杂的组织修复反应,其特征是诱导抗菌肽、伤口愈合细胞因子和上皮干细胞的修复性增殖。髓系和肠道上皮细胞中的炎症小体通过维持健康的微生物群来发挥这些作用。已经确定了与疾病相关的突变和某些炎症小体传感器的高表达。在许多情况下,抑制炎症小体的活性对实验性结肠炎小鼠模型的疾病结局有显著影响。在这里,我们讨论了不同炎症小体传感器在肠道稳态中的作用的最新研究,以及这些知识如何转化为治疗环境。