Cinnamaldehyde disrupts biofilm formation and swarming motility of Pseudomonas aeruginosa

Abstract

Bacterial biofilms can cause serious health care complications associated with increased morbidity and mortality. There is an urge to discover and develop new biofilm inhibitors from natural products or by modifying natural compounds or understanding the modes of action of existing compounds. Cinnamaldehyde (CAD), one of the major components of cinnamon oil, has been demonstrated to act as an antimicrobial agent against a number of Gram-negative and Gram-positive pathogens, including Pseudomonas aeruginosa, Helicobacter pylori and Listeria monocytogenes. Despite the mechanism of action of CAD against the model organism P. aeruginosa being undefined, based on its antimicrobial properties, we hypothesized that it may disrupt preformed biofilms of P. aeruginosa. The minimum inhibitory concentration (MIC) of CAD for planktonic P. aeruginosa was determined to be 11.8 mM. Membrane depolarization assays demonstrated disruption of the transmembrane potential of P. aeruginosa. CAD at 5.9 mM (0.5 MIC) disrupted preformed biofilms by 75.6 % and 3 mM CAD (0.25 MIC) reduced the intracellular concentrations of the secondary messenger, bis-(3'-5')-cyclic dimeric guanosine monophosphate (c-di-GMP), which controls P. aeruginosa biofilm formation. The swarming motility of P. aeruginosa was also reduced by CAD in a concentration-dependent manner. Collectively, these findings show that sub-MICs of CAD can disrupt biofilms and other surface colonization phenotypes through the modulation of intracellular signalling processes.

Antivirulence properties and related mechanisms of spice essential oils: A comprehensive review

“…c‐di‐GMP can transform from the planktonic to the sessile state to establish biofilm formation and promote the production of other virulence factors (Krasteva, Giglio, & Sondermann, 2012). Treatment with carvacrol at 1.5 mM (0.125 MIC) reduces 47.3% of preformed biofilm and 66.2% of c‐di‐GMP expression in P. aeruginosa PAO1, without evident killing of biofilm matrix‐embedded cells (Topa et al., 2018).…”

Activity of Cinnamaldehyde on Quorum Sensing and Biofilm Susceptibility to Antibiotics in Pseudomonas aeruginosa

“…Volumes of 100 µL of overnight MHB cultures of P. aeruginosa PAO1 adjusted to OD 600 of 0.1 were amended with 100 µL of 1:1 ratios of CAD-COL or CAD-TOB (50 µL of CAD + 50 µL of COL or TOB) to achieve final concentrations of 1.5 mM (CAD), 0.9 µM (COL) and 0.9 µM (TOB). The peg lid was added, and plates were incubated at 37 • C with shaking at 180 rpm for 6 h, which was determined to yield the maximum biofilm on the pegs [26]. Peg lids with adherent biofilms were transferred to a fresh plate base containing phosphate-buffered saline (PBS, 137 mM sodium chloride, 2.7 mM potassium chloride, 10 mM sodium phosphate dibasic and 2 mM potassium dihydrogen phosphate (Sigma-Aldrich, NSW, Australia)) to remove loosely attached bacterial cells.…”

“…In a previous study, we demonstrated that CAD can disrupt biofilms and other surface colonization phenotypes (e.g., swarming motility) of P. aeruginosa [26]. CAD also modulated intracellular signaling processes through decreasing cyclic-di-GMP levels [26], which led us to investigate whether CAD could be used as potential antivirulence compound [26]. A previous study with sublethal concentrations of CAD demonstrated inhibition of QS virulence factors and biofilm formation in P. fluorescence [27].…”

“…Cinnamaldehyde (CAD) is one of the primary phytoconstituents of cinnamon, with therapeutic potential to act as an antimicrobial agent against P. aeruginosa [24,25]. In a previous study, we demonstrated that CAD can disrupt biofilms and other surface colonization phenotypes (e.g., swarming motility) of P. aeruginosa [26]. CAD also modulated intracellular signaling processes through decreasing cyclic-di-GMP levels [26], which led us to investigate whether CAD could be used as potential antivirulence compound [26].…”

Antimicrobial Peptide‐Based Electrospun Fibers for Wound Healing Applications

“…In essence, once a pathogen reaches a specific cell density, signaling molecules called autoinducers begin to alter pathogen gene expression resulting in a colony forming a protective biofilm that is highly resistant to host defenses . The disruption of this process with agents known as quorum sensing inhibitors (QSI) can reduce the formation of biofilms, which allows host defenses and conventional therapies to be more effective, thus acting as a preventive or direct measure for counter‐acting pathogens in chronic wounds . QSI's can prevent the formation of biofilms in both gram positive and negative resistant pathogens such as P. aeruginosa and Burkholderia cenocepacia infections by disrupting the signal molecule N ‐acyl homoserine lactone in vivo .…”