Abstract
Manuka honey is a broad-spectrum antimicrobial agent that seems to affect different bacteria in many different ways. It has been shown to be bactericidal against Pseudomonas aeruginosa by destabilizing the cell wall, but we aimed to investigate whether there were further intracellular target sites. In this study inhibitory effects of manuka honey on P. aeruginosa were investigated using hydrophobicity assays, two-dimensional electrophoresis, quantitative RT-PCR, transmission electron microscopy and motility assays. Exposure of P. aeruginosa to manuka honey reduced both swarming and swimming motility. Moreover, this was a consequence of de-flagellation of the bacterial cell, which was correlated with decreased expression of the major structural flagellin protein, FliC, and concurrent suppression of flagellin-associated genes, including fliA, fliC, flhF, fleN, fleQ and fleR. The differential expression of the flagellar regulon in the presence of manuka honey was mapped schematically. Flagella are integral to bacterial adhesion, the initiation of infection and biofilm formation, and swarming has been associated with increased virulence. By limiting motility in vitro, we infer that manuka honey impacts on the virulence of P. aeruginosa. This deduction must now be tested in vivo.
Highlights
Pseudomonas aeruginosa is a Gram negative opportunistic pathogen that demonstrates exceptional environmental versatility and extensive antimicrobial resistance
This study aimed to investigate the effects of manuka honey on the motility of P. aeruginosa with a view to better understanding its potential to impact on virulence
Manuka honey results in consistently negative hydrophobicity In the modified MATH assay the adherence of untreated P. aeruginosa cells to n-hexadecane gradually increased over five hours (Fig. 1), indicating that hydrophobicity changed from negative to intermediate
Summary
Pseudomonas aeruginosa is a Gram negative opportunistic pathogen that demonstrates exceptional environmental versatility and extensive antimicrobial resistance. It has gained notoriety in nosocomial settings due to the emergence and persistence of multidrug resistant (MDR) strains. Between 1993 and 2002, for example, the number of multi-drug-resistant (MDR) strains isolated from intensive care units (ICUs) with resistance to >3 antimicrobials quadrupled (n = 13,999) and this trend has continued with time. P. aeruginosa has been implicated in both acute and chronic infections. Chronic venous leg ulcers that are colonised with P. aeruginosa exhibit a marked decrease in the success rate of skin grafts.[5]
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