This study investigated how antibiotics, to which Gluconacetobacter hansenii is naturally resistant, impact cellulose crystallinity, allomorph, aggregation into bundles and layers, cellulose yield, and cell morphology. G. hansenii was exposed to 100 μg/mL ampicillin, chloramphenicol, and kanamycin for 7 days, and cellulose structure was analyzed using scanning electron microscopy, X-ray diffraction, and Fourier transform infrared spectroscopy. Biomass and cellulose weights were also assessed. Ampicillin increased bundle thickness, and the bundles also showed nodular deposits indicative of non-cellulosic exopolysaccharide deposition. Ampicillin also yielded the lowest amount of cellulose per gram of biomass (p < 0.01) and induced significant filamentation behavior. Chloramphenicol inhibited biomass production (p < 0.01), increased the I-α allomorph content (p < 0.01), and also induced filamentation, though not as profusely as ampicillin. We hypothesize that defects in the peptidoglycan layer and in protein production lowered cellulose yield and promoted cells to undergo filamentation as a survival tactic. Additionally, we hypothesize that antibiotic stress caused additional exopolysaccharides to be produced and that they likely enhanced glucan chain aggregation into higher-order structures. Our findings have significant implications for downstream applications such as genetically engineering G. hansenii to produce bacterial cellulose with modified properties.
All Science Journal Classification (ASJC) codes
- Polymers and Plastics