Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review
Nanosilver Mitigates Biofilm Formation via FapC Amyloidosis Inhibition. / Huma, Zil-E; Javed, Ibrahim; Zhang, Zhenzhen et al.
In: Small (Weinheim an der Bergstrasse, Germany), Vol. 16, No. 21, 1906674, 05.2020.Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Journal article › Research › peer-review
}
TY - JOUR
T1 - Nanosilver Mitigates Biofilm Formation via FapC Amyloidosis Inhibition
AU - Huma, Zil-E
AU - Javed, Ibrahim
AU - Zhang, Zhenzhen
AU - Bilal, Hajira
AU - Sun, Yunxiang
AU - Hussain, Syed Zajif
AU - Davis, Thomas P
AU - Otzen, Daniel E
AU - Landersdorfer, Cornelia B
AU - Ding, Feng
AU - Hussain, Irshad
AU - Ke, Pu Chun
N1 - © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
PY - 2020/5
Y1 - 2020/5
N2 - Multidrug resistance of bacteria is a major challenge due to the wide-spread use of antibiotics. While a range of strategies have been developed in recent years, suppression of bacterial activity and virulence via their network of extracellular amyloid has rarely been explored, especially with nanomaterials. Here, silver nanoparticles and nanoclusters (AgNPs and AgNCs) capped with cationic branched polyethylenimine polymer are synthesized, and their antimicrobial potentials are determined at concentrations safe to mammalian cells. Compared with the ultrasmall AgNCs, AgNPs entail stronger binding to suppress the fibrillization of FapC, a major protein constituent of the extracellular amyloid matrix of Pseudomonas aeruginosa. Both types of nanoparticles exhibit concentration-dependent antibiofilm and antimicrobial properties against P. aeruginosa. At concentrations of 1 × 10-6 m or below, both the bactericidal activity of AgNCs and the antibiofilm capacity of AgNPs are associated with their structure-mediated bio-nano interactions but not ion release. For AgNPs, specifically, their antibiofilm potency correlates with their capacity of FapC fibrillization inhibition, but not with their bactericidal activity. This study demonstrates the antimicrobial potential of safe nanotechnology through the novel route of amyloidosis inhibition.
AB - Multidrug resistance of bacteria is a major challenge due to the wide-spread use of antibiotics. While a range of strategies have been developed in recent years, suppression of bacterial activity and virulence via their network of extracellular amyloid has rarely been explored, especially with nanomaterials. Here, silver nanoparticles and nanoclusters (AgNPs and AgNCs) capped with cationic branched polyethylenimine polymer are synthesized, and their antimicrobial potentials are determined at concentrations safe to mammalian cells. Compared with the ultrasmall AgNCs, AgNPs entail stronger binding to suppress the fibrillization of FapC, a major protein constituent of the extracellular amyloid matrix of Pseudomonas aeruginosa. Both types of nanoparticles exhibit concentration-dependent antibiofilm and antimicrobial properties against P. aeruginosa. At concentrations of 1 × 10-6 m or below, both the bactericidal activity of AgNCs and the antibiofilm capacity of AgNPs are associated with their structure-mediated bio-nano interactions but not ion release. For AgNPs, specifically, their antibiofilm potency correlates with their capacity of FapC fibrillization inhibition, but not with their bactericidal activity. This study demonstrates the antimicrobial potential of safe nanotechnology through the novel route of amyloidosis inhibition.
KW - FapC
KW - amyloids
KW - antibiofilms
KW - silver nanoclusters
KW - silver nanoparticles
KW - FIBRIL FORMATION
KW - GOLD NANOPARTICLES
KW - BACTERIA
KW - DISCRETE MOLECULAR-DYNAMICS
KW - SILVER NANOPARTICLES
KW - NANOCLUSTERS
KW - OXIDE NANOPARTICLES
KW - ANTIBACTERIAL ACTIVITY
KW - PSEUDOMONAS-AERUGINOSA
KW - EFFICIENT
U2 - 10.1002/smll.201906674
DO - 10.1002/smll.201906674
M3 - Journal article
C2 - 31984626
VL - 16
JO - Small
JF - Small
SN - 1613-6810
IS - 21
M1 - 1906674
ER -