Helicobacter pylori plays a key role in gastric adenocarcinoma induced by spasmolytic polypeptide-expressing metaplasia  

作　　者：Mian-Li Li Xin-Xin Hong Wei-Jian Zhang Yi-Zhong Liang Tian-Tian Cai Yi-Fei Xu Hua-Feng Pan Jian-Yuan Kang Shao-Ju Guo Hai-Wen Li 

机构地区：[1]Department of Gastroenterology,Shenzhen Hospital of Integrated,Traditional Chinese and Western Medicine,Shenzhen 518033,Guangdong Province,China [2]Department of Gastroenterology,Shenzhen Traditional Chinese Medicine Hospital,Shenzhen 518033,Guangdong Province,China [3]Science and Technology Innovation Center,Guangzhou University of Traditional Chinese Medicine,Guangzhou 510405,Guangdong Province,China

出　　处：《World Journal of Clinical Cases》2023年第16期3714-3724,共11页世界临床病例杂志

基　　金：Supported by the Guangdong Basic and Applied Basic Research Foundation,No.2020A1515110947;the National Natural Science Foundation of China,No.82104747;the Scientific Research Project of Guangdong Bureau of Traditional Chinese Medicine,No.20231303;the Guangdong Provincial Key Research and Development Plan,No.2020B1111100011.

摘　　要：Heliobacter pylori(H. pylori), a group 1 human gastric carcinogen, is significantly associated with chronic gastritis, gastric mucosal atrophy, and gastric cancer.Approximately 20% of patients infected with H. pylori develop precancerous lesions, among which metaplasia is the most critical. Except for intestinal metaplasia(IM), which is characterized by goblet cells appearing in the stomach glands, one type of mucous cell metaplasia, spasmolytic polypeptide-expressing metaplasia(SPEM), has attracted much attention. Epidemiological and clinicopathological studies suggest that SPEM may be more strongly linked to gastric adenocarcinoma than IM. SPEM, characterized by abnormal expression of trefoil factor 2, mucin 6, and Griffonia simplicifolia lectin II in the deep glands of the stomach, is caused by acute injury or inflammation. Although it is generally believed that the loss of parietal cells alone is a sufficient and direct cause of SPEM, further in-depth studies have revealed the critical role of immunosignals.There is controversy regarding whether SPEM cells originate from the transdifferentiation of mature chief cells or professional progenitors. SPEM plays a functional role in the repair of gastric epithelial injury. However, chronic inflammation and immune responses caused by H. pylori infection can induce further progression of SPEM to IM, dysplasia, and adenocarcinoma. SPEM cells upregulate the expression of whey acidic protein 4-disulfide core domain protein 2 and CD44 variant 9, which recruit M2 macrophages to the wound. Studies have revealed that interleukin-33, the most significantly upregulated cytokine in macrophages, promotes SPEM toward more advanced metaplasia. Overall, more effort is needed to reveal the specific mechanism of SPEM malignant progression driven by H.pylori infection.

关 键 词：Gastric cancers Helicobacter pylori Intestinal metaplasia Macrophages Spasmolytic polypeptide-expressing metaplasia 

分 类 号：R735.2[医药卫生—肿瘤]