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Publications

Journal Article Ppublish 1 citation

PubMed: 40893413 DOI: 10.1016/j.onano.2025.100240

Microbicidal mechanisms for light-activated molecular nanomachines in Mycobacterium smegmatis: A model for pathogenic bacteria.

OpenNano 23

Authors: Thushara Galbadage, Dongdong Liu, James M Tour, Jeffrey D Cirillo, Richard S Gunasekera

Affiliations

  • Department of Microbial Pathogenesis and Immunology, Texas A&M University, School of Medicine, Bryan, TX, USA.
  • Department of Chemistry Rice University, Houston, TX, USA.
  • Department of Materials Science and NanoEngineering, Rice University, Houston, TX, USA.
  • Smalley-Curl Institute, Rice University, Houston, TX, USA.
  • NanoCarbon Center, Rice University, Houston, TX, USA.
  • Department of Chemistry, Rice University, Houston, TX, USA.
  • Center for Airborne Pathogens Research and Imaging, Texas A&M Institute for Genome Sciences and Society, Bryan, TX, USA.
  • Department of Chemistry and Biochemistry, Biola University, La Mirada, CA, USA.

Abstract

There is a global health crisis of antimicrobial resistance, responsible for over a million deaths annually. Mycobacterial infections are a major contributor to this crisis, causing more deaths than any other single infectious agent. Notably, the rise of multidrug-resistant (MDR), extensively drug-resistant (XDR), and totally drug-resistant (TDR) strains of Mycobacterium tuberculosis has led to higher mortality rates and challenge all existing antibiotic regimens. Light-activated molecular nanomachines (MNMs) represent a promising class of broad-spectrum antimicrobial agents that could help counter this rise in antimicrobial resistance. Addressing a key knowledge gap, this study explores the mechanisms of action for MNMs in Mycobacterium smegmatis, a surrogate model for pathogenic mycobacteria. We show that fast-rotor MNMs significantly reduce bacterial viability, achieving up to 97 % reduction in M. smegmatis with 30 minutes of light activation when compared to non-activated MNM 1 (p < 0.0001, t = 24.55), as determined by an unpaired t-test. Using fluorescence and confocal microscopy, we also show the colocalization of MNM 1 with M. smegmatis as part of their mechanism of action. The ability to translate these observations to pathogenic mycobacteria was demonstrated by the ability of MNM 1 to kill 93.5 % of M. tuberculosis with 5 minutes of light activation when compared to non-activated MNM 1 (p < 0.0001, t = 19.24). These findings suggest that MNMs have the potential to be innovative and sustainable antimicrobial agents for the treatment of pathogenic mycobacterial infections.

MeSH

Mycobacterium, Pharmaceutical Preparations, Tuberculosis, Mycobacterium Smegmatis, Bacteria, Infections