Silica |
72.4 ± 8.2 nm, quasi-spherical |
Polymyxin B, Vancomycin |
Positively charged polymyxin B and vancomycin adsorbs in the cylindrical holes of negatively charged bare-MSNs and carboxyl modified MSNs via electrostatic interactions. Pore size and available surface area inside the holes determine the concentration of antibiotics to be absorbed. |
Staphylococcus Aureus (DSM 20231) Escherichia Coli (K12 DSM498–0714-001) Pseudomonas aeruginosa (PAO1 DSM 19880) Klebsiella oxytoca (DSM 5175) Acinetobacter Baumannii (DSM 30006) |
Outer cell membrane |
Synergistic activity of polymyxin B and vancomycin increase the antibiotic potency both on gram-positive and gram-negative bacteria. Polymyxin B interacts with Gram-negative bacteria’s outer membrane; Van disrupts peptidoglycan synthesis. The lower release rate of carboxyl loaded MSNs (containing higher net negative charge) enhances the antibacterial efficacy by the increased local concentration of immobilized antibiotics. |
Gounani et al. (2019)
|
Silica core-shell |
277 ± 12 nm, spherical |
Gentamicin sulfate and sodium rifamycin |
Positively charged gentamicin adhesion on the silica core NPs (first antibiotic loading). Three OH groups of gentamicin favor this interaction on the silica surface by hydrogen bond formation. The shell functionalization with thiol (R-SH) group favors negatively-charged rifamycin sorption on the outer surface like a shell layer (second antibiotic loading). |
Staphylococcus aureus (ATCC29213), Pseudomonas aeruginosa (ATCC27853) |
Cell membrane |
Two oppositely charged antibiotics can be delivered using the silica core-shell NP, with different release kinetics of two drug molecules. Rifamycin is rapidly desorbed; on the other hand, gentamicin requires a longer time to release and follow a slow diffusion pattern. For Gram-positives, core-shell NP can deliver dual antibiotics effectively and show 1.5 × more potency than a single antibiotic. |
Mebert et al. (2016)
|
Mesoporous silica NPs (MSNs) with Cu (II) and Ni (II) complexes |
<100 nm, spherical |
Gentamicin |
NH2 and COO- groups of gentamicin interact with the free coordination sites of Cu (II) and Ni (II) complexes supported on MSNs nanochannels, resulting in gentamicin’s high adsorption. |
Staphylococcus aureus (ATCC6538), Bacillus subtilis (ATCC6633), Pseudomonas aeruginosa (ATCC9027), Escherichia coli (ATCC25922) |
Cell membrane |
Tiny, porous structures of metal-MSNs complexes enable high adsorption of gentamicin, and as a drug carrier delivers increased gentamicin in the cell membrane. Also, they facilitate enzyme immobilization. |
Tahmasbi et al. (2018)
|
Ordered mesoporous silica NPs (OMSNs) |
100 nm, Non-spherical (oblate) |
Isoniazid (INH) |
INH encapsulates into the hollow oblate structures of OMSNs, and functionalization with trehalose sugar provides specific targeting ability to mycobacteria |
Mycobacterium smegmatis mc2 651 |
Cell wall |
Enhanced interactions of INH loaded OMSNs with the bacterial cell. The OMSNs have anisotropic morphology, low density, high surface-to-volume ratio, and large hollow interior capacity that enhance cell binding efficiency (adhere to bacterial cell surfaces), cellular uptake kinetics, high drug-encapsulation capacities, sustained drug release, and increased interactions of particles with bacteria. |
Hao et al. (2015)
|
Carbon |
Pore size 5.8 and 13.9 nm, wall thickness 25 and 45 nm, spherical |
Vancomycin |
Intrinsic hydrophobicity of mesoporous hollow carbon (MHC) allows higher vancomycin loading capacity in the porous nanospheres. By adjusting the pore size and wall thickness of MHC, vancomycin adsorption and release rate can be controlled. |
Escherichia. coli, Staphylococcus epidermidis
|
Cell membrane |
The combination of specific pore size and the wall thickness of MHC nanospheres contain higher vancomycin loading by physisorption and sustained drug release capacity over a long time to inhibit bacterial peptidoglycan synthesis. Adhesion of hydrophobic MHC nanospheres disrupts the cell membrane, followed by inserting vancomycin inside the cell. |
Nor et al. (2016)
|
Titania-silica composites |
Fiber or rope-like structures |
Oxytetracycline (OTC) |
Titania ions in silica wall surface create strong donor-acceptor bonds with OTC molecules. |
Staphylococcus aureus (ATCC25923), Escherichia coli (ATCC25922) Pseudomonas aeruginosa (ATCC27853) |
Cell membrane |
Mesoporous crystalline titania on the silica surface allows slower OTC release for a sustained period inducing a burst effect. |
Georgescu et al. (2017)
|
Silica NPs |
50–80 nm, spherical |
Tetracycline (TC) |
Silica-tetracycline composites (SiO2-TC) forms by the silanol (Si-O-H) group’s interaction with TC molecules inside silica pores. |
TC/Amp resistantEscherichia coli, TC resistant Escherichia coli
|
Cell membrane lipopolysaccharides |
TC NPs interact with lipopolysaccharides (create hydrogen bonds between saccharides and hydroxyl groups) and destabilize the silica surface’s peptidoglycan layer. TC stops protein synthesis by binding with the 30S ribosome subunit. |
Capeletti et al. (2014)
|