Nanoparticle binding attenuates the pathobiology of gastric cancer-associated Helicobacter pylori.
Nanoparticle binding attenuates the pathobiology of gastric cancer-associated Helicobacter pylori.
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DOI：
10.1039/c7nr06573f
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发表时间：
2018-01
期刊：
影响因子：
6.7
通讯作者：
Dana Westmeier;Gernot Posselt;Angelina Hahlbrock;S. Bartfeld;Cecilia Vallet;C. Abfalter;D. Docter;S. Knauer;S. Wessler;R. Stauber
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文献类型：
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作者：
Dana Westmeier;Gernot Posselt;Angelina Hahlbrock;S. Bartfeld;Cecilia Vallet;C. Abfalter;D. Docter;S. Knauer;S. Wessler;R. Stauber
肠道细菌可能会导致严重的疾病，包括与胃癌相关的幽门螺杆菌。它们的感染途径与口服胃肠吸收纳米颗粒的途径重叠，在环境或消费者/医疗暴露期间越来越多地发生。通过活细胞荧光、电子以及原子力显微镜和元素分析等综合独立分析方法，我们发现广泛的纳米颗粒(NPs)而不是微粒与幽门螺杆菌和肠道病原体形成复合体，而不需要特定的官能化。NP的快速组装不受生理温度变化的影响，但受NP的物理化学性质的影响。对于表面带负电荷的小NPs，可以观察到结合能力的提高，而表面‘隐形’修饰可以降低结合能力。利用人胃上皮细胞和胃的3D-有机物模型，我们表明NP涂层不能抑制幽门螺杆菌的细胞附着。然而，即使是非杀菌二氧化硅纳米颗粒的组装也通过减少CagA磷酸化、细胞骨架重排和IL-8的分泌来减轻幽门螺杆菌的感染。在这里，我们证明了NP与肠道细菌的结合可能会影响他们的病理生物学，这可以被进一步利用来通过纳米材料合理地调节微生物的(病理)生物学。
Enteric bacteria may cause severe diseases, including gastric cancer-associated Helicobacter pylori. Their infection paths overlap with the oro-gastrointestinal uptake route for nanoparticles, increasingly occurring during environmental or consumer/medical exposure. By comprehensive independent analytical methods, such as live cell fluorescence, electron as well as atomic force microscopy and elemental analysis, we show that a wide array of nanoparticles (NPs) but not microparticles form complexes with H. pylori and enteric pathogens without the need for specific functionalization. The NP-assembly that occurred rapidly was not influenced by variations in physiological temperature, though affected by the NPs' physico-chemical characteristics. Improved binding was observed for small NPs with a negative surface charge, whereas binding could be reduced by surface 'stealth' modifications. Employing human gastric epithelial cells and 3D-organoid models of the stomach, we show that NP-coating did not inhibit H. pylori's cellular attachment. However, even the assembly of non-bactericidal silica NPs attenuated H. pylori infection by reducing CagA phosphorylation, cytoskeletal rearrangement, and IL-8 secretion. Here we demonstrate that NP binding to enteric bacteria may impact their pathobiology which could be further exploited to rationally modulate the (patho)biology of microbes by nanomaterials.