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.

有机体适应性要求适当的反应以抵消感染或伤害带来的威胁。在哺乳动物的肠上皮屏障处，炎性小体协调了精细的组织修复反应，其特征在于诱导了抗菌肽，伤口愈合的细胞因子和上皮干细胞的修复性增殖。骨髓和肠上皮区室中的炎性体部分地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性体传感器的表达升高。在许多情况下，在实验性结肠炎的小鼠模型中，炎性体活性的抑制对疾病结局具有显着影响。这里，