da Silva Tatley Fernanda, Aldwell Frank E, Dunbier Anita K, Guilford Parry J
Cancer Genetics Laboratory, Department of Biochemistry, University of Otago, Dunedin, Aotearoa, New Zealand.
Infect Immun. 2003 Mar;71(3):1580-3. doi: 10.1128/IAI.71.3.1580-1583.2003.
The observation that E-cadherin is the principal epithelial receptor for the bacterial pathogen Listeria monocytogenes led us to investigate whether N-terminal fragments of E-cadherin containing the L. monocytogenes binding domain could inhibit entry of the bacteria into cultured epithelial cells. Here we demonstrate that a conditioned medium from a gastric cancer cell line (Kato III) that carries a truncating CDH-1 mutation 3' of the L. monocytogenes binding domain can inhibit the uptake of the bacteria into Caco-2 cells. The inhibitory activity of the Kato III conditioned medium could be mimicked by incubation of the bacteria with a recombinant 26-kDa N-terminal E-cadherin peptide prior to infection. Furthermore, these data suggest that cleavage of the 80-kDa extracellular domain of E-cadherin from the cell surface may provide an innate form of pathogen defense by acting as a decoy receptor for L. monocytogenes.
E-钙黏蛋白是细菌病原体单核细胞增生李斯特菌的主要上皮受体，这一发现促使我们研究含有单核细胞增生李斯特菌结合域的E-钙黏蛋白N端片段是否能够抑制该细菌进入培养的上皮细胞。在此，我们证明，携带单核细胞增生李斯特菌结合域3'端截短型CDH-1突变的胃癌细胞系（Kato III）的条件培养基能够抑制该细菌进入Caco-2细胞。在感染前，用重组26 kDa的N端E-钙黏蛋白肽孵育细菌，可模拟Kato III条件培养基的抑制活性。此外，这些数据表明，从细胞表面切割下80 kDa的E-钙黏蛋白胞外域，可能通过充当单核细胞增生李斯特菌的诱饵受体，提供一种先天性的病原体防御形式。
