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Nanoscale. 2018 Jan 18;10(3):1453-1463. doi: 10.1039/c7nr06573f.

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

Author information

1
Department of Nanobiomedicine/ENT, University Medical Center of Mainz, Langenbeckstrasse 1, 55101 Mainz, Germany. roland.stauber@unimedizin-mainz.de danawestmeier@uni-mainz.de.

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 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.

PMID:
29303193
DOI:
10.1039/c7nr06573f
[Indexed for MEDLINE]

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