Chronic wound infections are often difficult to prevent and a hassle to treat. Fortunately, Sarah Maddocks and her colleagues from Cardiff Metropolitan University recently published a study that suggests the effectiveness of manuka honey in both treating bacterial infections and preventing them in the first place.
Various strains of bacteria are naturally found on skin. Streptococcus pyogenes, for example, is a species of spherical bacteria commonly found in healthy humans. When the skin is damaged, however, the open wound provides an entry through which this strain of bacteria can enter. The subsequent interaction between the bacteria and protein matrix may result in a non-healing chronic wound.
After the bacteria gain access to the protein matrix within the wound, they begin adhering to the host's protein ligands via cell-wall-anchored adhesins. This promotes bacterial cell aggregation, which results in the formation of biofilms.
Biofilms are matrixes of extracellular polymeric substance produced by the bacteria. They bind to surfaces in order to facilitate bacterial adhesion. When formed in open wounds, biofilms provide bacteria with the advantage of antibiotic resistance. Since antibiotics cannot penetrate the biofilm to reach the bacteria, physicians often have trouble treating infected wounds.
Fortunately, studies show that honey both destroys biofilms and even prevents their initial formation. Although the antimicrobial properties of honey have long been known, the mechanisms through which honey performs its feat have always been a mystery.
The study Maddocks conducted aimed to determine the in vitro effect of honey against biofilm, and the specific interactions by which honey exerts its effect. In the experiment, S. pyogenes cultures were treated with manuka honey. Various procedures were performed to determine the effect of honey on biofilm and bacterial cells.
Results show that honey was able to completely eradicate existing biofilms. Furthermore, honey seemed to prevent the aggregation of bacterial cells initially, thus preventing the formation of biofilm.
This study newly demonstrates that honey exerts its effects by preventing the binding of bacterial cells to secreted human fibronectin. Fibronectin is a protein in the extracellular matrix. It plays a crucial role in wound healing. Large amounts of this protein are deposited in open wounds to aid clot formation.
PCR results suggest that honey interrupts bacterial binding by reducing the expression of adhesins on bacterial cell surfaces. This in turn lowers the amount of interaction between bacteria and the open wound, thus preventing biofilm formation.
Reduction in isolated amounts of RNA suggests that perhaps honey affects bacteria cells at a transcriptional level. This could further indicate the possibility of additional genes, besides the surface adhesins, being differently expressed. However, this area requires further investigation.
Honey's high osmolarity and low water activity is also thought to contribute to an environment unsuitable for bacterial growth. Moreover, honey provides the added advantage by reducing the risk of bacterial resistance even to repeated exposure of high dose honey application.
Maddocks' lab continues to study other wound bacteria common to wound infections. Findings from this study offer a cheaper and more effective way toward treating wound infections. Hopefully, these results can extend to other species of bacteria as well, further contributing to existing antibiotic therapies.
