The Role of Metallic Nanoparticles in Inhibition of Mycobacterium Tuberculosis and Enhances Phagosome Maturation into the Infected Macrophage

Abstract

This review focuses on the role of gallium (Ga) nanoparticles (NPs) to enhance phagosome maturation into the Mycobacterium tuberculosis-infected macrophage and the role of magnetic iron NPs as nanocarriers of antituberculosis drugs. The literature shows that silver (Ag) and zinc oxide (ZnO) NPs with dimensions less than 10 nm can penetrate directly through the macrophage bilayer membrane. Ag NPs increase the permeability membrane by motiving the aggregation of proteins in the periplasmic space and forming nano-sized pores. ZnO NPs can interact with the membrane of M. tuberculosis, which leads to the formation of surface pores and the release of intracellular nucleotides. The colloidal Ag:ZnO mixture NPs with 1:1 ratio can eliminate M. tuberculosis and shows the lowest cytotoxicity effects on MCF-7 and THP-1 cell lines. Ag/ZnO nanocrystals are not able to kill M. tuberculosis alone ex-vivo. Hence, bimetallic gold (Au)/Ag NPs possessed high efficiency to inhibit M. tuberculosis in an ex-vivo THP-1 infection model. Co-delivery of mixed MeNPs into a polymeric carrier collaborated to selective uptake by macrophages through passive targeting, initial burst release of ions from the encapsulated metallic (Me) NPs, and eventually, reduction of MeNPs toxicity, and plays a pivotal role in increasing the antitubercular activity compared to use alone. In addition, Ga NPs can import drugs to the macrophage, inhibit M. tuberculosis growth, and reduce the inhibition of phagosome maturation. Magnetic encapsulated NPs exhibited good drug release properties and might be suitable as carriers of antituberculosis drugs.

Keywords