Epithelial maturity influences EPEC-induced desmosomal alterations.
Epithelial maturity influences EPEC-induced desmosomal alterations.
复制标题
上皮成熟度影响 EPEC 诱导的桥粒改变。
DOI：
10.1080/19490976.2018.1506669
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发表时间：
2019
期刊：
影响因子：
12.2
通讯作者：
Viswanathan,VK
中科院分区：
文献类型：
--
作者：
Roxas,JenniferLising;Vedantam,Gayatri;Viswanathan,VK
桥粒是一种连接蛋白复合物，它赋予邻近宿主细胞强大的粘附能力。在最近的一项研究中，我们发现肠致病性大肠杆菌（EPEC）破坏桥粒，削弱细胞间粘附，扰乱肠上皮（C2BBe）细胞的屏障功能。桥粒损伤依赖于EPEC效应蛋白EspH及其对Rho GTP酶的抑制作用。EspH介导的Rho失活导致角蛋白中间丝的收缩和桥粒钙粘蛋白的降解。EPEC感染的C2BBe细胞的免疫荧光研究显示，角蛋白向细胞核的收缩与桥粒钙粘蛋白桥粒芯糖蛋白-2（DSG 2）的显著细胞质再分布一致。在本附录中，我们扩展了EPEC诱导的角蛋白收缩如何导致DSG 2锚定在连接处的丢失，并表明上皮细胞单层的成熟影响感染期间桥粒的命运。
Desmosomes are junctional protein complexes that confer strong adhesive capacity to adjacent host cells. In a recent study, we showed that enteropathogenicEscherichia coli(EPEC) disrupts desmosomes, weakens cell-cell adhesion and perturbs barrier function of intestinal epithelial (C2BBe) cells. Desmosomal damage was dependent on the EPEC effector protein EspH and its inhibitory effect on Rho GTPases. EspH-mediated Rho inactivation resulted in retraction of keratin intermediate filaments and degradation of desmosomal cadherins. Immunofluorescence studies of EPEC-infected C2BBecells revealed keratin retraction towards the nucleus coincident with significant cytoplasmic redistribution of the desmosomal cadherin desmoglein-2 (DSG2). In this addendum, we expand on how EPEC-induced keratin retraction leads to loss of DSG2 anchoring at the junctions, and show that maturity of the epithelial cell monolayer impacts the fate of desmosomes during infection.