The Role of Inflammation in Regulating Gastric Metaplasia

摘要 本申请解决的知识空白是癌前病变（即化生）是如何发生的， 随后引发胃腺癌。幽门螺杆菌（Helicobacter pylori，H.幽门）和 自身免疫性胃炎会导致慢性炎症并增加胃癌的风险。本申请 包括许多小鼠模型和人体组织样本，以研究免疫细胞的重要性。 (mast细胞和Th2 T细胞）和细胞因子（IL 4和IL 13）在诱导胃上皮化生和促进胃上皮化生中的作用。 胃上皮化生和肿瘤发生的发展。识别炎症细胞和启动炎症反应的信号 化生和驱动肿瘤发展可以提高识别个体的能力， 疾病进展，以及预防和治疗肿瘤前病变相关的新的免疫策略 包括胃癌在内的胃部疾病

ABSTRACT The knowledge gaps this application addresses are how precancerous lesions (i.e. metaplasia) arise and subsequently fuel adenocarcinoma of the stomach. Infection with Helicobacter pylori (H. pylori) and autoimmune gastritis both cause chronic inflammation and increase the risk of gastric cancer. This application includes numerous mouse models and human tissue samples to investigate the importance of immune cells (mast cells and Th2 T cells) and cytokines (IL4 and IL13) in inducing gastric metaplasia and promoting the development of gastric metaplasia and tumorigenesis. Identifying inflammatory cells and signals that initiate metaplasia and drive tumor development could improve the ability to identify individuals at an increased risk of disease progression, and new immune based strategies to prevent and treat preneoplastic lesions associated with gastric diseases, including gastric cancer.