Aspirin inhibits the growth of Helicobacter pylori and enhances its susceptibility to antimicrobial agents

Abstract

Background and aim: The role of Helicobacter pylori and aspirin in peptic ulcer formation and recurrence remains an important clinical topic. The interaction between aspirin and H pylori in vitro is also not clear. We investigated the effect of aspirin on the growth of H pylori and on the susceptibility of H pylori to antimicrobials. Methods: Time killing studies of H pylori were performed with different concentrations of aspirin and salicylate. Growth of bacteria was assessed spectrophotometrically and by viable colony count. The effects of aspirin on the efficiency of colony formation and on metronidazole induced mutation to rifampicin resistance in H pylori were determined. Minimal inhibitory concentrations (MICs) of aspirin and metronidazole were tested by the standard agar dilution method. MICs of amoxycillin and clarithromycin were determined by the E test method. Results: Aspirin and salicylate inhibited the growth of H pylori in a dose dependent manner and bactericidal activity was due to cell lysis. Aspirin 400 µg/ml caused a 2 logs decrease in colony forming units/ml at 48 hours, and suppressed the normal ability of metronidazole to induce new mutations to rifampicin. The IC 90 of aspirin was 512 µg/ml. Increased susceptibility of amoxycillin, clarithromycin, and metronidazole to H pylori was observed at 1 mM (180 µg/ml) aspirin. Conclusions: Aspirin inhibited the growth of H pylori, suppressed the mutagenic effect of metronidazole, and enhanced the susceptibility of H pylori to antimicrobial agents. This mechanism is important in future drug development for effective clearing and overcoming resistance.

The assessment of the antibacterial and antifungal activities of aspirin, EDTA and aspirin-EDTA combination and their effectiveness as antibiofilm agents

“…These effects include changes in membrane potentials and virulence factors production, reduction in extracellular polysaccharide and prostaglandin production (Price et al 2000;Wang et al 2003;Alem and Douglas 2004). These effects contribute to aspirin's antimicrobial activities against planktonic and biofilm cultures.…”

“…In vitro studies on planktonic cultures demonstrated aspirin's antifungal (Stepanovic et al 2004), antibacterial (Nicolau et al 1995;Wang et al 2003) and antiviral (Mazur et al 2007) activities. Clinically, aspirin treatment was associated with a significant decrease in risk of Staphylococcus aureus bacteraemia (Sedlacek et al 2007).…”

“…For each well showing no turbidity, 10 ll was transferred and added to 100 ll of saline, or 1 mol l )1 of CaCl 2 (SD Fine-Chem Ltd, Biosar, India) to neutralize aspirin and EDTA by dilution and chelation, respectively (Wang et al 2003;Harrison et al 2007). The entire volume was spread onto nutrient agar plate.…”

Evaluation of antibacterial activity of some non-steroidal anti-inflammatory drugs against Escherichia coli causing urinary tract infection

“…NSAIDs are commonly used medicines for the treatment of pain and inflammation. Many studies found that some NSAIDs have good antibacterial activity especially diclofenac sodium (Wang et al, 2003). In this study, some NSAIDs (diclofenac sodium, aspirin, indomethacin and ibuprofen) were tested against a total of 48 isolates of E. coli.…”

“…All these drugs with moderate to powerful anti-microbial activities have been known as "non-antibiotics" (Dastidar et al, 2000). Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used medicines for pain and inflammation management and previous studies have revealed that some NSAIDs have antibacterial activity (Wang et al, 2003;Hersh et al, 1991). NSAIDs exhibited strong antimicrobial activity when tested against a large number of Gram-positive and negative bacteria and the MIC ranged from 50-200 µg/mL in most of the cases and even lower in some cases (Annadurai et al, 1998;Sukul et al, 2015;Obad et al, 2015).…”