Autophay-inducing agent shown to neutralize tularemia

A recent study in the Journal of Biomedical Science has revealed that an autophagy-inducing agent introduced to the bacteria that causes tularemia in humans can eradicate the small-molecule agents that target innate immunity.

Autophay plays an important role in the intracellular survival of several pathogenic bacteria. For the study, AR-12, an autophagy-inducing agent introduced on Francisella tularensis - the causative bacterium of tularemia in humans and a potential bioterrorism agent - was found to induce autophagy in THP-1 macrophages, which was indicated by an increase in autophagosome formations.

AR-12 also potently inhibited F. tularensis' intraceullular survival as well as Francisella novicida in macrophages in association with increased bacterial co-localization with autophagosomes.

Intracellular F. novidica's effect was fully reversed by AR-12 in the presence of 3-methyl adenine, an autophagy inhibitor, or chloroquine, the lysosome inhibitor.

Intracellular F. novicida was also shown to not be susceptible to AR-12's inhibitory activity when added 12 hours post-infection in THP-1 macrophages. This lack of susceptibility was shown to be independent of the intracellular location of bacteria.

The results of the study have shown that the AR-12 autophagy-inducing agent can effectively be used to eradicate tularemia's small-molecule agents, an important step in creating biodefenses for what is considered a viable bioweapon.