Department of Biochemistry and Food Chemistry, University of Turku, Turku, Finland.
PLoS One. 2013 Jul 31;8(7):e70509. doi: 10.1371/journal.pone.0070509. Print 2013.
Aggregatibacter actinomycetemcomitans is a gram-negative opportunistic oral pathogen. It is frequently associated with subgingival biofilms of both chronic and aggressive periodontitis, and the diseased sites of the periodontium exhibit increased levels of the proinflammatory mediator interleukin (IL)-1β. Some bacterial species can alter their physiological properties as a result of sensing IL-1β. We have recently shown that this cytokine localizes to the cytoplasm of A. actinomycetemcomitans in co-cultures with organotypic gingival mucosa. However, current knowledge about the mechanism underlying bacterial IL-1β sensing is still limited. In this study, we characterized the interaction of A. actinomycetemcomitans total membrane protein with IL-1β through electrophoretic mobility shift assays. The interacting protein, which we have designated bacterial interleukin receptor I (BilRI), was identified through mass spectrometry and was found to be Pasteurellaceae specific. Based on the results obtained using protein function prediction tools, this protein localizes to the outer membrane and contains a typical lipoprotein signal sequence. All six tested biofilm cultures of clinical A. actinomycetemcomitans strains expressed the protein according to phage display-derived antibody detection. Moreover, proteinase K treatment of whole A. actinomycetemcomitans cells eliminated BilRI forms that were outer membrane specific, as determined through immunoblotting. The protein was overexpressed in Escherichia coli in both the outer membrane-associated form and a soluble cytoplasmic form. When assessed using flow cytometry, the BilRI-overexpressing E. coli cells were observed to bind 2.5 times more biotinylated-IL-1β than the control cells, as detected with avidin-FITC. Overexpression of BilRI did not cause binding of a biotinylated negative control protein. In a microplate assay, soluble BilRI bound to IL-1β, but this binding was not specific, as a control protein for IL-1β also interacted with BilRI. Our findings suggest that A. actinomycetemcomitans expresses an IL-1β-binding surface-exposed lipoprotein that may be part of the bacterial IL-1β-sensing system.
伴放线放线杆菌是一种革兰氏阴性机会性病原体。它常与慢性和侵袭性牙周炎的龈下生物膜有关,牙周病部位的促炎介质白细胞介素(IL)-1β水平升高。一些细菌物种可以通过感应 IL-1β来改变其生理特性。我们最近表明,这种细胞因子在与器官型牙龈黏膜的共培养物中定位于放线共生放线杆菌的细胞质中。然而,目前关于细菌 IL-1β感应机制的知识仍然有限。在这项研究中,我们通过电泳迁移率变动分析来描述放线共生放线杆菌总膜蛋白与 IL-1β的相互作用。通过质谱鉴定出相互作用的蛋白质,我们将其命名为细菌白细胞介素受体 I(BilRI),并发现它是巴斯德氏菌科特有的。根据蛋白功能预测工具获得的结果,该蛋白定位于外膜,并且含有典型的脂蛋白信号序列。根据噬菌体展示衍生抗体检测,所有 6 株临床放线共生放线杆菌生物膜培养物均表达该蛋白。此外,用蛋白水解酶处理整个放线共生放线杆菌细胞消除了BilRI 形式,该形式是通过免疫印迹确定的外膜特异性。该蛋白在大肠杆菌中外膜相关形式和可溶性细胞质形式中均过表达。当使用流式细胞术评估时,BilRI 过表达的大肠杆菌细胞与对照细胞相比,结合生物素化-IL-1β的能力增加了 2.5 倍,该检测使用 avidin-FITC 进行。BilRI 的过表达不会导致结合生物素化的阴性对照蛋白。在微孔板测定中,可溶性 BilRI 与 IL-1β结合,但这种结合不是特异性的,因为 IL-1β的对照蛋白也与 BilRI 相互作用。我们的研究结果表明,放线共生放线杆菌表达一种与白细胞介素结合的表面暴露脂蛋白,可能是细菌白细胞介素 1β感应系统的一部分。