Nanomaterials Aiming to Tackle Antibiotic-Resistant Bacteria

Abstract

The global health of humans is seriously affected by the dramatic increases in the resistance patterns of antimicrobials against virulent bacteria. From the statements released by the Centers for Disease Control and Prevention about the world entering a post-antibiotic era, and forecasts about human mortality due to bacterial infection being increased compared to cancer, the current body of literature indicates that emerging tools such as nanoparticles can be used against lethal infections caused by bacteria. Furthermore, a different concept of nanomaterial-based methods can cope with the hindrance faced by common antimicrobials, such as resistance to antibiotics. The current review focuses on different approaches to inhibiting bacterial infection using nanoparticles and aiding in the fabrication of antimicrobial nanotherapeutics by emphasizing the functionality of nanomaterial surface design and fabrication for antimicrobial cargo.

Keywords: antibiotic resistance; antimicrobial nanomaterial; bacterial biofilm; metallic nanoparticle; multidrug-resistant bacteria.

Figure 1

Structural difference between Gram-positive and Gram-negative bacteria.

Figure 2

Scheme of mechanistic action of antimicrobial materials to combat microbial resistance. Adapted from [6], Dove Medical Press, 2020.

Figure 3

Illustration of a possible multivalent interaction between a Van-capped Au nanoparticle (2) and a VanA genotype VRE strain (hexagons: glycosides; ellipses represent the amino acid residues of the glycanpeptidyl precursor with different colors: L-Ala (yellow), D-Glu (orange), L-Lys (green), D-Ala (blue), and D-Lac (purple)). Adapted with permission from [25], American Chemical Society, 2003.

Figure 4

(A) Molecular structures of functional ligands on AuNPs. (B) MIC values (nM) of AuNPs bearing different hydrophobic surface ligands against laboratory E. coli DH5R. Log P represents the calculated hydrophobic values of the end groups. (C) PI staining showing NP 3 (C10-AuNP)-induced bacterial cell membrane damage. Scale bar is 5 μm. (D) Hemolytic activity of NP 3 at different concentrations. HC50 was estimated to be ∼400 nM (as denoted by the red cross in figure). Adapted with permission from [28], American Chemical Society, 2014.

Figure 5

(A) Schematic of on-site precipitation method for the synthesis of dual action antibacterial composite material, AgBr/NPVP poly(4-vinylpyridine)-co-poly(4-vinyl-N-hexylpyridinium bromide). Adapted with permission from [31], published by American Chemical Society, 2006. (B) Schematic Illustration of the Synthetic Procedure for SiO2−Ag/PRh Nanoparticles (C) FTIR and (D) UV−vis spectra of rhodanine monomer (black solid line) and SiO₂−Ag/PRh nanoparticles (red dotted line). (D,E) Antibacterial assessment of four different particles (pristine silica, thiol-silane-treated silica, SiO₂−Ag, and SiO₂−Ag/PRh) dispersed in solution and blank water toward E. coli and (F) S. aureus with or without silver-ion scavenger (100 μL of neutralizer solution) at pH 7.4. Adapted with permission from [33], American Chemical Society, 2013.

Figure 6

(A) Schematic charge conversion of PEG-b-PCL-bPAE/Van nanoparticles due to pH. Zeta potential (B) and in vitro Van release (C) profiles of PEG-b-PCL/Van and PEG-b-PCLb-PAE/Van nanoparticles under different pH conditions (n = 4). (D) In vitro stability of PEG-b-PCL-b-PAE/Van nanoparticles in PBS buffer (0.01 M) for 24 h. (E) In vivo fluorescence images of inflammation-bearing mice after 2 h, 12 h and 24 h of Van injection and (F) statistical analysis and (G) representative CLSM images of cutaneous inflammation slices from inflammation-bearing mice after 24 h of Van injection. (n = 3, ** p < 0.01). Adapted with permission from [51], Royal Society of Chemistry, 2016.