The capacity of pathogenic microorganisms to adhere to host cells and avoid clearance by the host immune system is the initial and most decisive step leading to infections. Bacteria have developed different strategies to attach to diverse host surface structures. One important strategy is the adhesion to extracellular matrix (ECM) proteins (e.g., collagen, fibronectin, laminin) that are highly abundant in connective tissue and basement membranes. Gram-negative bacteria express variable outer membrane proteins (adhesins) to attach to the host and to initiate the process of infection. Understanding the underlying molecular mechanisms of bacterial adhesion is a prerequisite for targeting this interaction by “anti-ligands” to prevent colonization or infection of the host. Future development of such “anti-ligands” (specifically interfering with bacteria-host matrix interactions) might result in the development of a new class of anti-infective drugs for the therapy of infections caused by multidrug-resistant Gram-negative bacteria. This review summarizes our current knowledge about the manifold interactions of adhesins expressed by Gram-negative bacteria with ECM proteins and the use of this information for the generation of novel therapeutic antivirulence strategies.

中文翻译：

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与宿主的相互作用：纤连蛋白和细胞外基质蛋白在革兰氏阴性细菌粘附中的作用。

病原微生物附着于宿主细胞并避免被宿主免疫系统清除的能力是导致感染的最初也是最决定性的步骤。细菌已经开发出不同的策略来附着到不同的宿主表面结构。一种重要的策略是粘附至结缔组织和基底膜中高度丰富的细胞外基质（ECM）蛋白（例如胶原蛋白，纤连蛋白，层粘连蛋白）。革兰氏阴性细菌表达可变的外膜蛋白（粘附素）以附着于宿主并启动感染过程。了解细菌粘附的基本分子机制是通过“抗配体”靶向这种相互作用以防止宿主定植或感染的前提。这种“抗配体”的未来发展（特别是干扰细菌与宿主基质的相互作用）可能会导致开发出一种新型的抗感染药物，用于治疗由多重耐药的革兰氏阴性细菌引起的感染。这篇综述总结了我们当前有关革兰氏阴性细菌表达的粘附素与ECM蛋白的多种相互作用的知识，以及该信息在产生新型治疗性抗病毒策略中的应用。