Université de Strasbourg, CNRS, RIDI UPR 9022, 67000 Strasbourg, France.
Université de Strasbourg, CNRS, RIDI UPR 9022, 67000 Strasbourg, France.
Cell Host Microbe. 2016 Dec 14;20(6):716-730. doi: 10.1016/j.chom.2016.10.010. Epub 2016 Nov 23.
Besides digesting nutrients, the gut protects the host against invasion by pathogens. Enterocytes may be subjected to damage by both microbial and host defensive responses, causing their death. Here, we report a rapid epithelial response that alleviates infection stress and protects the enterocytes from the action of microbial virulence factors. Intestinal epithelia exposed to hemolysin, a pore-forming toxin secreted by Serratia marcescens, undergo an evolutionarily conserved process of thinning followed by the recovery of their initial thickness within a few hours. In response to hemolysin attack, Drosophila melanogaster enterocytes extrude most of their apical cytoplasm, including damaged organelles such as mitochondria, yet do not lyse. We identify two secreted peptides, the expression of which requires CyclinJ, that mediate the recovery phase in which enterocytes regain their original shape and volume. Epithelial thinning and recovery constitute a fast and efficient response to intestinal infections, with pore-forming toxins acting as alarm signals.
除了消化营养物质,肠道还能保护宿主免受病原体的侵害。肠细胞可能会受到微生物和宿主防御反应的损伤,导致其死亡。在这里,我们报告了一种快速的上皮反应,它可以减轻感染应激,保护肠细胞免受微生物毒力因子的作用。暴露于溶血素的肠上皮经历了一个进化保守的过程,即变薄,然后在数小时内恢复到最初的厚度。在溶血素攻击下,果蝇肠细胞挤出大部分顶端细胞质,包括受损的细胞器,如线粒体,但不会裂解。我们鉴定出两种分泌肽,其表达需要 CyclinJ,介导肠细胞恢复到原始形状和体积的恢复阶段。上皮变薄和恢复是对肠道感染的快速有效的反应,而形成孔的毒素则作为警报信号。