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Doxycycline induces Hok toxin killing in host E. coli
Chinwe Uzoma Chukwudi1,2, Liam Good2
1Department of Veterinary Pathology and Microbiology, University of Nigeria, Nsukka, Nigeria.
Plos One
|July 7, 2020
Summary
Doxycycline increases susceptibility to bacterial death in bacteria carrying the hok/sok locus, a common element in multi-drug resistance plasmids. This suggests doxycycline can inhibit plasmid stability and pathogenicity, potentially combating antimicrobial resistance.
Area of Science:
- Microbiology
- Molecular Biology
- Antimicrobial Resistance
Background:
- Tetracycline antibiotic efficacy is declining due to resistance.
- The hok/sok locus, a type I toxin/antitoxin element, is linked to multi-drug resistance plasmids and enhances bacterial survival and pathogenicity.
- Doxycycline can bind double-stranded RNA (dsRNA) and inhibit its processing by RNase III.
Purpose of the Study:
- To investigate the antibacterial activity of doxycycline against bacteria harboring the hok/sok locus.
- To determine the effects of doxycycline on hok/sok-induced growth changes and the underlying mechanisms.
Main Methods:
- Diverse E. coli strains were transformed with hok/sok plasmids.
- Susceptibility to doxycycline and growth changes were assessed.
- Phenotypic characteristics of bacterial death were analyzed.
Main Results:
- The hok/sok locus increased bacterial susceptibility to doxycycline, particularly in strains with pronounced hok/sok-induced growth effects.
- This increased susceptibility occurred despite the beta-lactam resistance conferred by the hok/sok locus.
- Doxycycline induced bacterial death resembling Hok toxin expression, suggesting inhibition of dsRNA degradation.
Conclusions:
- Doxycycline inhibits the degradation of hok/sok toxin/antitoxin dsRNA, leading to Hok toxin expression and bacterial cell death.
- Doxycycline may counteract plasmid maintenance, propagation, persistence, and pathogenicity mechanisms associated with the hok/sok locus.
- This finding offers a potential strategy to mitigate the rise of antimicrobial resistance.
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