Kernbauer Elisabeth, Cadwell Ken
aKimmel Center for Biology and Medicine at the Skirball Institute bDepartment of Microbiology, New York University School of Medicine, New York, New York, USA.
Curr Opin Gastroenterol. 2014 Nov;30(6):539-46. doi: 10.1097/MOG.0000000000000121.
To highlight recent findings that identify an essential role for the cellular degradative pathway of autophagy in governing a balanced response to intestinal pathogens and commensals.
Following the genetic association of autophagy with inflammatory bowel disease susceptibility, increasing evidence indicates that this pathway functions in various epithelial lineages to support the intestinal barrier. New studies are also revealing that autophagy proteins dictate the quality and magnitude of immune responses. Mouse models, in particular, suggest that autophagy and inflammatory bowel disease susceptibility genes regulate inflammatory responses to viruses, a finding that coincides with an increasing appreciation that viruses have intricate interactions with the host and the microbiota beyond the obvious host-pathogen relationship.
Autophagy and other immunological or stress response pathways intersect in mucosal immunity to dictate the response to pathogenic and commensal agents. The development of novel treatment strategies, as well as prognostic and diagnostic tools for gastrointestinal disorders, will be greatly facilitated by a deeper understanding of these interactions at the cell type and microbe-specific manner, which includes less appreciated components of the microbiota, such as eukaryotic and prokaryotic viruses.
强调近期研究发现，即细胞自噬降解途径在调节对肠道病原体和共生菌的平衡反应中起关键作用。
自噬与炎症性肠病易感性存在基因关联后，越来越多的证据表明该途径在多种上皮细胞谱系中发挥作用以维持肠道屏障。新研究还表明自噬蛋白决定免疫反应的质量和强度。特别是小鼠模型显示，自噬和炎症性肠病易感基因调节对病毒的炎症反应，这一发现与人们越来越认识到病毒除了明显的宿主-病原体关系外，还与宿主和微生物群有复杂相互作用相吻合。
自噬与其他免疫或应激反应途径在黏膜免疫中相互交叉，以决定对病原体和共生菌的反应。深入了解细胞类型和微生物特异性方式下的这些相互作用，包括微生物群中较少被认识的成分，如真核和原核病毒，将极大地促进胃肠道疾病新治疗策略以及预后和诊断工具的开发。
