Dr. Weeks’ Comment: Years ago in Vermont, here I trained (and where 30 years ago I became a beekeeper), family docs doing house calls through ominous snowdrifts to care for patients living far from hospitals dressed surgical wounds with raw honey. Since those days, science has come a long way and honey, as a remedy, has kept up! Cheap and safe and effective “centisble” raw honey merits more respect. Now we learn that hone inhibits the formation of biofilms which are the tenacious film that helps pathogens resist antibiotics or anti-fungal drugs. “Got infection? Get Honey!”
“…This is the first time that a topical antimicrobial of any type has been documented to inhibit binding to a host protein…”
- Honey curtails biofilm formation
- Researchers study effects on S. progenies cultures
- Concentration of 5 percent inhibits aggregation of cells
International report — Researchers in the lab have shown for the first time that at least one type of honey, a substance used by traditional healers for centuries, can inhibit pathogen binding and the formation of a biofilm.
Manuka honey applied as a topical antimicrobial downregulates genes in the pathogen that produce the binding proteins, according to investigators at Cardiff Metropolitan University in the United Kingdom.
This is the first time that a topical antimicrobial of any type has been documented to inhibit binding to a host protein,” says microbiologist Sarah E. Maddocks, Ph.D., who sought to better understand the mechanisms behind honey’s activity.
Honey has been used throughout history to treat wounds. Researchers have documented its broad-spectrum antibacterial activity against more than 80 species of bacteria. Much of that is attributed to honey’s high osmolarity, low water activity and hydrogen peroxide. Manuka honey is unique in that it also contains reactive methylglyoxal, a potent protein-glycating agent, at levels up to 100-fold higher than found in conventional honeys.
Dr. Maddocks conducted the first systematic analysis of the effect of medical-grade manuka honey on developing and established biofilms. She initially focused on Streptococcus pyogenes.
Streptococci are key components of the commensal microbiota that colonizes the skin. Normally benign, streptococci are more threatening when the barrier function of the skin is breeched. The bacteria can enter a wound site, initiate infection, destroy skin grafts, and persist as a biofilm. Variants of the genus differ in their capacity to form disruptive biofilms, but they all share a common initial mechanism of adhesion to a substratum.
Dr. Maddocks grew the bacteria in wells of microtiter plates and exposed it to dilutions of manuka honey at various concentrations of weight/volume.
Growth of the planktonic form of S. pyogenes was inhibited and the overall number of cells was reduced at a 20 percent concentration of honey (the Minimum Inhibitory Concentration, or MIC), while the minimum bactericidal concentration (MBC) was 40 percent. No pathogens could be recovered after an eight-hour incubation with a 45 percent concentration of honey, she told Dermatology Times.
Low concentrations work.
Another experiment found that concentrations of the honey as low as 5 percent completely inhibited intercellular aggregation of the bacteria. It reduced the formation of biofilms in a dose-dependent manner.
“Cells exposed to 20 percent manuka honey showed no evidence of microcolony formation and contained only long chains of cells, some of which were enlarged,” Dr. Maddocks says.
Established biofilms of S. pyogenes were somewhat more resistant to the antimicrobial effect, but, again, a dose response was observed. Two hours after application of the honey there was a reduction in the biomass; 10 percent concentration/72 percent reduction, 20 percent concentration/77 percent reduction, 40 percent concentration/85 percent reduction (p=0.01).
Dr. Maddocks’ work establishes for the first time that manuka honey reduced S. pyogenes binding to fibronectin. High levels of fibronectin are generated during wound healing. It also is one of the preferential ligands for pathogen attachment to the host wound site. There was no statistically significant reduction in binding to fibrinogen.
A closer look found significantly reduced expression of two key fibronectin-binding proteins produced by S. pyogenes. There was a 31 percent reduction of expression of the gene sfbI in the presence of a 20 percent concentration of the honey, while expression of the genes of was reduced below the level of detection. She says, “This is the first time that a topical antimicrobial of any type has been documented to inhibit binding to a host protein.”
Dr. Maddocks has begun to look at other pathogens such as methicillin-resistantStaphylococcus aureus and Pseudomonas aeruginosa, which also commonly infect wounds. “So far we are seeing different mechanisms of action to those that we observed for S. pyogenes,” she says.
THANKS to Dr. Saul Pilar for sending this article!