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Nanoparticle binding attenuates the pathobiology of gastric cancer-associated Helicobacter pylori

Abstract

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 of specific functionalization. NP-assembly 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 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 assembly of non-bactericidal silica NPs attenuated H. pylori infection by reducing CagA phosphorylation, cytoskeletal rearrangement, and IL-8 secretion. We here 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.

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Supplementary files

Publication details

The article was received on 04 Sep 2017, accepted on 04 Dec 2017 and first published on 05 Dec 2017


Article type: Paper
DOI: 10.1039/C7NR06573F
Citation: Nanoscale, 2017, Accepted Manuscript
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    Nanoparticle binding attenuates the pathobiology of gastric cancer-associated Helicobacter pylori

    D. Westmeier, G. Posselt, A. Hahlbrock, S. Bartfeld, C. Vallet, C. Abfalter, D. Docter, S. Knauer, S. Wessler and R. H. Stauber, Nanoscale, 2017, Accepted Manuscript , DOI: 10.1039/C7NR06573F

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