Abstract
The human intestinal microbiota varies in composition among individuals and is largely influenced by external factors such as diet, drugs and environment. While it is well-known to play a pivotal role in maintaining gut health, its interactions with non-antibiotic pharmaceuticals remain understudied. This in vitro study evaluates the effects of over-the-counter (OTC) aspirin (Cardiprin) on the growth dynamics of three commensal gut bacterial strains, Escherichia coli, Klebsiella pneumoniae and Enterococcus faecalis. Employing a dual-method approach of disk diffusion assay (DDA) and colony-forming unit (CFU) analysis, the study evaluates aspirin’s effects at physiologically relevant (300 µg/mL) and high (1000 µg/mL) concentrations. DDA demonstrated consistent inhibition zones across all strains and highlighted aspirin’s weak antibacterial potency, while CFU analyses revealed strain-specific responses. At 300 µg/mL of aspirin, E. coli and E. faecalis exhibited growth comparable to baseline while K. pneumoniae uniquely showed enhanced growth. However, at a higher concentration of 1000 µg/mL, growth of all strains were inhibited to different extents. These results underscore the need for further investigation into the therapeutic and unintended effects of oral aspirin on gut microbial growth.
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Abstract
The human intestinal microbiota varies in composition among individuals and is largely influenced by external factors such as diet, drugs and environment. While it is well-known to play a pivotal role in maintaining gut health, its interactions with non-antibiotic pharmaceuticals remain understudied. This in vitro study evaluates the effects of over-the-counter (OTC) aspirin (Cardiprin) on the growth dynamics of three commensal gut bacterial strains, Escherichia coli, Klebsiella pneumoniae and Enterococcus faecalis. Employing a dual-method approach of disk diffusion assay (DDA) and colony-forming unit (CFU) analysis, the study evaluates aspirin’s effects at physiologically relevant (300 µg/mL) and high (1000 µg/mL) concentrations. DDA demonstrated consistent inhibition zones across all strains and highlighted aspirin’s weak antibacterial potency, while CFU analyses revealed strain-specific responses. At 300 µg/mL of aspirin, E. coli and E. faecalis exhibited growth comparable to baseline while K. pneumoniae uniquely showed enhanced growth. However, at a higher concentration of 1000 µg/mL, growth of all strains were inhibited to different extents. These results underscore the need for further investigation into the therapeutic and unintended effects of oral aspirin on gut microbial growth.
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