Abstract：
Gastroenteritis is inflammation of the lining of stomach and intestines and causes significant morbidity and mortality worldwide. Many viruses, especially RNA viruses are the most common cause of enteritis. Innate immunity is the first line of host defense against enteric RNA viruses and virus-induced intestinal inflammation. The first layer of defense against enteric RNA viruses in the intestinal tract is intestinal epithelial cells (IECs), dendritic cells and macrophages under the intestinal epithelium. These innate immune cells express pathogen-recognition receptors (PRRs) for recognizing enteric RNA viruses through sensing viral pathogen-associated molecular patterns (PAMPs). As a result of this recognition type I interferon (IFN), type III IFN and inflammasome activation occurs, which function cooperatively to clear infection and reduce viral-induced intestinal inflammation. In this review, we summarize recent findings about mechanisms involved in enteric RNA virus-induced intestinal inflammation. We will provide an overview of the enteric RNA viruses, their RNA sensing mechanisms by host PRRs, and signaling pathways triggered by host PRRs, which shape the intestinal immune response to maintain intestinal homeostasis.
摘要：
胃肠炎是胃和肠壁的炎症,在世界范围内引起显著的发病率和死亡率。许多病毒,尤其是RNA病毒是肠炎的最常见原因。先天性免疫是宿主防御肠道RNA病毒和病毒诱导的肠道炎症的第一道防线。肠道中防御肠RNA病毒的第一层是肠上皮细胞（IECs），肠上皮下的树突状细胞和巨噬细胞。这些先天免疫细胞表达病原体识别受体（PRR），用于通过感知病毒病原体相关分子模式（PAMP）来识别肠道RNA病毒。由于这种识别I型干扰素（IFN），发生III型IFN和炎性体激活，它们协同作用以清除感染并减少病毒引起的肠道炎症。在这次审查中,我们总结了有关肠道RNA病毒诱导的肠道炎症机制的最新发现。我们将提供肠RNA病毒的概述，它们通过宿主PRR的RNA传感机制，和由宿主PRR触发的信号通路，形成肠道免疫反应以维持肠道稳态。
