Figure 1.

Schematic drawing presenting a hypothetical model describing differences in the potential of antibiotics to generate the spiral-to-coccoid transformation in H. pylori. In the routine therapy of H. pylori, the following antibiotics are used: rifampicin (transcription), tetracycline and clarithromycin (translation), metronidazole and levofloxacin (the DNA structure or replication), and amoxicillin (the cell wall) (Jones et al., 2008; Francesco, 2011; Nishizawa and Suzuki, 2014). Based on reports showing the ability of bactericidal antibiotics to stimulate oxidative stress in microbial cells (Kohanski et al., 2007; Brynildsen et al., 2013; Dwyer et al., 2014; Belenky et al., 2015; Lobritz et al., 2015; Li et al., 2017) and the results of Mortaji et al. (2020), demonstrating the oxidative stress-dependent induction of the toxin-antitoxin system in H. pylori, a hypothetical model integrating the above observations has been proposed. Antibiotics acting on transcription and translation (rifampicin, tetracycline or clarithromycin) have a marginal effect on the oxido-reductive state of bacterial cells and therefore do not significantly affect the toxin-antitoxin balance. The opposite situation is suggested for antibiotics targeting the cell wall or DNA (amoxicillin, levofloxacin or metronidazole), all of which stimulate the accumulation of reactive oxygen species in bacterial cells and the oxidative stress-related disturbance of the toxin-antitoxin balance in favor of the former. The increased production of this toxin is accompanied by the conversion of H. pylori into spherical forms.