Determining if the Manuka Honey Iron Chelation Mechanism is Effective Against Pseudomonas aeruginosa Biofilm Formation
Faculty Mentor
Andrea Castillo
Presentation Type
Poster
Start Date
4-14-2026 2:00 PM
End Date
4-14-2026 4:00 PM
Location
PUB NCR
Primary Discipline of Presentation
Biology
Abstract
Pseudomonas aeruginosa is a highly adaptable facultative anaerobic bacterium that causes skin and lung infections in immunocompromised individuals. Pseudomonas aeruginosa can form communities called biofilms, and is intrinsically resistant to many antibiotics, making it a serious threat in healthcare settings. Biofilms can form on many surfaces, such as sinks, ventilators, and dialysis tubes, creating a persistent reservoir for infections. The P. aeruginosa biofilm matrix, composed of polysaccharides, DNA, and protein, provides the bacteria with increased resistance to antibiotics, UV radiation, pH changes, and immune system attacks. Bacteria in biofilms can cause chronic and challenging to treat infections. Manuka Honey (MH) is a promising antimicrobial due to its broad-spectrum activity, even against multi-drug-resistant pathogens, like P. aeruginosa. This broad-spectrum activity is due to the multiple antimicrobial mechanisms of MH. Our research group previously identified iron chelation—where the essential macronutrient iron is made unavailable to bacteria—as one of the MH antimicrobial mechanisms. We hypothesize that MH will inhibit P. aeruginosa biofilm formation through the mechanism of iron chelation. In these experiments, biofilm formation in the presence of MH, with or without iron supplementation, will be compared to untreated samples. Biofilm formation will be based on crystal violet dye binding and quantified using a spectrophotometer. When P. aeruginosa was incubated with sub-minimum inhibitory (MIC) MH concentrations (15% and 18%), reduction in biofilm formation was observed (P < 0.0001 and P < 0.01, respectively). The reduction in biofilm formation corresponds with the reduction in cell number (P < 0.001 and P < 0.0001, respectively). In next steps, MH treated P. aeruginosa will be supplemented with iron to determine whether restoring iron availability restores bacterial biofilm formation. Future studies will also assess the impact of MH on preformed biofilms, to evaluate whether MH can disrupt established biofilm communities.
Recommended Citation
Nunez, Isaac, "Determining if the Manuka Honey Iron Chelation Mechanism is Effective Against Pseudomonas aeruginosa Biofilm Formation" (2026). 2026 Symposium. 22.
https://dc.ewu.edu/srcw_2026/ps_2026/p3_2026/22
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Determining if the Manuka Honey Iron Chelation Mechanism is Effective Against Pseudomonas aeruginosa Biofilm Formation
PUB NCR
Pseudomonas aeruginosa is a highly adaptable facultative anaerobic bacterium that causes skin and lung infections in immunocompromised individuals. Pseudomonas aeruginosa can form communities called biofilms, and is intrinsically resistant to many antibiotics, making it a serious threat in healthcare settings. Biofilms can form on many surfaces, such as sinks, ventilators, and dialysis tubes, creating a persistent reservoir for infections. The P. aeruginosa biofilm matrix, composed of polysaccharides, DNA, and protein, provides the bacteria with increased resistance to antibiotics, UV radiation, pH changes, and immune system attacks. Bacteria in biofilms can cause chronic and challenging to treat infections. Manuka Honey (MH) is a promising antimicrobial due to its broad-spectrum activity, even against multi-drug-resistant pathogens, like P. aeruginosa. This broad-spectrum activity is due to the multiple antimicrobial mechanisms of MH. Our research group previously identified iron chelation—where the essential macronutrient iron is made unavailable to bacteria—as one of the MH antimicrobial mechanisms. We hypothesize that MH will inhibit P. aeruginosa biofilm formation through the mechanism of iron chelation. In these experiments, biofilm formation in the presence of MH, with or without iron supplementation, will be compared to untreated samples. Biofilm formation will be based on crystal violet dye binding and quantified using a spectrophotometer. When P. aeruginosa was incubated with sub-minimum inhibitory (MIC) MH concentrations (15% and 18%), reduction in biofilm formation was observed (P < 0.0001 and P < 0.01, respectively). The reduction in biofilm formation corresponds with the reduction in cell number (P < 0.001 and P < 0.0001, respectively). In next steps, MH treated P. aeruginosa will be supplemented with iron to determine whether restoring iron availability restores bacterial biofilm formation. Future studies will also assess the impact of MH on preformed biofilms, to evaluate whether MH can disrupt established biofilm communities.