Targeting the apical junctional complex during acute bacterial infections can be detrimental for the host in several aspects. First, the rupture of the epithelium or endothelium integrity is toxic in itself. In addition, extracellular bacterial pathogens or bacterial toxins can cross the body's physical barriers using the paracellular route and induce infection or intoxication of distant organs. No single strategy has been developed to disrupt junctional structures, rather each bacterium has its own method, which can be classed in one of the following three categories: (i) proteolysis/perturbation of adhesive proteins involved in tight or adherens junctions by bacterial or toxin-activated eukaryotic proteases, (ii) manipulation of host regulatory pathways leading to weakened intercellular adhesion, or (iii) delocalization of the junctional complex to open the gateway toward the subepithelial compartment. In this review, examples of each of these mechanisms are provided to illustrate how creative bacteria can be when seeking to disrupt cell-cell junctions.

中文翻译：

---

细菌病原体靶向顶端连接复合物。

在急性细菌感染期间靶向顶端连接复合物可能在多个方面对宿主有害。首先，上皮破裂或内皮完整性本身就是有毒的。此外，细胞外细菌病原体或细菌毒素可通过细胞旁途径穿越人体的物理屏障，并引起远处器官的感染或中毒。尚未开发出破坏连接结构的单一策略，而是每种细菌都有自己的方法，可以将其归为以下三类之一：（i）细菌或毒素对参与紧密连接或粘附连接的粘附蛋白进行蛋白水解/微扰活化的真核蛋白酶，（ii）操纵导致细胞间粘附减弱的宿主调节途径，或（iii）交界复合体离域，以打开通往上皮下隔室的通道。在这篇综述中，提供了每种机制的实例，以说明试图破坏细胞-细胞连接时创造性细菌的表现。