The homing receptor CD44 is involved in the progression of precancerous gastric lesions in patients infected with Helicobacter pylori and in development of mucous metaplasia in mice.
The homing receptor CD44 is involved in the progression of precancerous gastric lesions in patients infected with Helicobacter pylori and in development of mucous metaplasia in mice.
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DOI：
10.1016/j.canlet.2015.10.037
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发表时间：
2016-02-01
期刊：
影响因子：
9.7
通讯作者：
Zabaleta J
中科院分区：
文献类型：
--
作者：
Garay J;Piazuelo MB;Majumdar S;Li L;Trillo-Tinoco J;Del Valle L;Schneider BG;Delgado AG;Wilson KT;Correa P;Zabaleta J
幽门螺杆菌（Helicobacter pylori，H.幽门螺杆菌）导致炎症事件，可以促进胃癌的发展。免疫细胞通过其受体和配体在内皮区室中的相互作用从循环转移到感染的粘膜中。CD 44表达在进展期胃病变中增加。然而，这种分子与这些病变随时间推移的进展的关联尚未研究。此外，对导致胃炎和可能导致胃癌的CD 44依赖性细胞过程缺乏了解。我们在这里学习H。pylori阳性受试者的胃病变范围从多灶性萎缩性胃炎到异型增生，以确定基因表达的变化与疾病进展超过6年的时间。我们报告，CD 44的表达显着增加，在个人的胃病变进展沿着胃癌前级联反应。我们还表明，CD 44 −/−小鼠发展不太严重和不太广泛的H。pylori诱导的化生，并且与野生型小鼠相比显示较少的浸润性Gr 1+细胞。我们目前的数据表明，CD 44与疾病进展相关。与这些作用相关的机制包括干扰素γ应答的诱导。
Infection with Helicobacter pylori (H. pylori) leads to inflammatory events that can promote gastric cancer development. Immune cells transition from the circulation into the infected mucosa through the interaction of their receptors and ligands in the endothelial compartment. CD44 expression is increased in advanced gastric lesions. However, the association of this molecule with the progression of these lesions over time has not been investigated. In addition, there is a lack of understanding of the CD44-dependent cellular processes that lead to gastritis, and possibly to gastric cancer. Here we studied H. pylori-positive subjects with gastric lesions that ranged from multifocal atrophic gastritis to dysplasia to determine gene expression changes associated with disease progression over a period of six years. We report that CD44 expression is significantly increased in individuals whose gastric lesions progressed along the gastric precancerous cascade. We also show that CD44−/− mice develop less severe and less extensive H. pylori-induced metaplasia, and show fewer infiltrating Gr1+ cells compared to wild type mice. We present data suggesting that CD44 is associated with disease progression. Mechanisms associated with these effects include induction of interferon gamma responses.