<p>Silver Nanoparticles for the Therapy of Tuberculosis</p>

Abstract

Rapid emergence of aggressive, multidrug-resistant Mycobacteria strain represents the main cause of the current antimycobacterial-drug crisis and status of tuberculosis (TB) as a major global health problem. The relatively low-output of newly approved antibiotics contributes to the current orientation of research towards alternative antibacterial molecules such as advanced materials. Nanotechnology and nanoparticle research offers several exciting new-concepts and strategies which may prove to be valuable tools in improving the TB therapy. A new paradigm in antituberculous therapy using silver nanoparticles has the potential to overcome the medical limitations imposed in TB treatment by the drug resistance which is commonly reported for most of the current organic antibiotics. There is no doubt that AgNPs are promising future therapeutics for the medication of mycobacterial-induced diseases but the viability of this complementary strategy depends on overcoming several critical therapeutic issues as, poor delivery, variable intramacrophagic antimycobacterial efficiency, and residual toxicity. In this paper, we provide an overview of the pathology of mycobacterial-induced diseases, andhighlight the advantages and limitations of silver nanoparticles (AgNPs) in TB treatment.

Mycogenic Metal Nanoparticles for the Treatment of Mycobacterioses

“…One should also note that the conjunction of biomolecules such as peptides or chitosan results in increased antimycobacterial activity, but this effect is limited after mycobacteria are internalized by macrophages [ 7 ]. More effective strategies rely on combining NPs with classical anti-TB therapeutics that ensure both extra- and intracellular activity, although only a few in vivo studies have explored this option [ 7 ].…”

“…This will allow us to understand and manipulate all caveats regarding their synthesis and antimicrobial mode of action, and standardize synthesis methodologies to attain best scale-up yields. Furthermore, as mentioned by Tăbăran et al [ 7 ] in relation to AgNPs, there are a few other therapeutic obstacles to overcome: “poor delivery, variable intramacrophagic antimycobacterial efficiency, and residual toxicity”. The same applies to all other MNPs effective against mycobacteria.…”

“…Despite their similarities, NTM have lower human pathogenicity than mycobacteria from the Mycobacterium tuberculosis (MTb) complex [ 6 , 7 ] (species with 85–100% DNA homology with MTb, which include M. africanum, M. bovis, M. caprae, M. canetti, M. pinnipedii, M. tuberculosis, M. microti, or M. mungi , which are all pathogenic [ 3 , 7 , 8 ]). The fact that NTM share many infectious traits with the causing agents of tuberculosis (TB) allows them to be used in many research studies as model organisms of infection for this disease, with the advantage of being less pathogenic and faster growing species [ 7 , 9 ].…”

“…MTb, the causing agent of TB in humans, is particularly deadly due to some of its differentiating characteristics: (1) thick cell wall composed of peptidoglycan, arabinoglalactans, and mycolic acids; (2) slow growth rate; (3) ability to persist in non-replicating form for a long period; (4) capacity to cause latent-infection; (5) easy development of drug resistance; and (6) drug tolerance [ 11 , 12 ]. The main virulence factors responsible for these characteristics are: lipoarabinomannan (LAM), mannose-capped-LAM, lipomannan (LM), cord factor (Trehalose-6,6-dimycolate–TDM), phosphatidylinositol mannosides (PIMs), phthiocerol dimycocerosates (PDIM), phenolic glycolipids (PGLs), twin-arginine translocation (TAT) system, exported repetitive protein (Erp), and proteins from the ESAT-6 family [ 7 ].…”

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“…It generally targets lungs but can harm other organs as well. In India, almost 50% of patients are suffering, and one person dies from TB every minute 19 . However, due to the consumption of antibiotics, the challenge of multidrug-resistant TB has increased drastically.…”