期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 596, 期 17, 页码 3861-3867出版社
WILEY
DOI: 10.1113/JP275512
关键词
SPEM; spasmolytic polypeptide-expressing metaplasia; macrophage polarization; IL-13; IL-33; ST2; transdifferentiation
资金
- Department of Veterans Affairs Merit Review Award [I01BX000930]
- Department of Defense IDEA grant [CA160479]
- NIH [RO1 DK071590, T32 GM008554]
The development of intestinal-type gastric cancer is preceded by the emergence of metaplastic cell lineages in the gastric mucosa. In particular, intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia (SPEM) have been associated with the pathological progression to intestinal-type gastric cancer. The development of SPEM represents a physiological response to damage that recruits reparative cells to sites of mucosal injury. Metaplastic cell lineages are characterized by mucus secretion, adding a protective barrier to the epithelium. Increasing evidence indicates that the influence of alarmins and cytokines is required to initiate the process of metaplasia development. In particular, IL-33 derived from epithelial cells stimulates IL-13 production by specialized innate immune cells to induce chief cell transdifferentiation into SPEM following the loss of parietal cells from the corpus of the stomach. While SPEM represents a physiological healing response to acute injury, persistent injury and chronic inflammation can perpetuate a recurring pattern of reprogramming and metaplasia that is a risk factor for gastric cancer development. The transdifferentiation of zymogen secreting cells into mucous cell metaplasia may represent both a general repair mechanism in response to mucosal injury in many epithelia as well as a common pre-neoplastic pathway associated with chronic injury and inflammation.
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