Lehrstuhl Zellbiologie, Fachbereich Biologie, Universität Konstanz, 78457 Konstanz, Germany.
Science. 2010 Sep 3;329(5996):1197-201. doi: 10.1126/science.1190892.
Colonization of mucosal surfaces is the key initial step in most bacterial infections. One mechanism protecting the mucosa is the rapid shedding of epithelial cells, also termed exfoliation, but it is unclear how pathogens counteract this process. We found that carcinoembryonic antigen (CEA)-binding bacteria colonized the urogenital tract of CEA transgenic mice, but not of wild-type mice, by suppressing exfoliation of mucosal cells. CEA binding triggered de novo expression of the transforming growth factor receptor CD105, changing focal adhesion composition and activating beta1 integrins. This manipulation of integrin inside-out signaling promotes efficient mucosal colonization and represents a potential target to prevent or cure bacterial infections.
黏膜表面的定植是大多数细菌感染的关键初始步骤。一种保护黏膜的机制是上皮细胞的快速脱落,也称为脱屑,但不清楚病原体如何对抗这一过程。我们发现癌胚抗原(CEA)结合细菌通过抑制黏膜细胞脱屑而定植于 CEA 转基因小鼠的泌尿生殖道,但不定植于野生型小鼠。CEA 结合触发转化生长因子受体 CD105 的新表达,改变焦点黏附组成并激活β1 整合素。这种对整合素内外信号的操纵促进了有效的黏膜定植,代表了预防或治疗细菌感染的潜在目标。