A new study published by scientists at the Dr. Rath Research Institute examines how theaflavin-3,3′-digallate (TF3), a compound from black tea, can inhibit the effects of a toxin produced by Staphylococcus aureus (S. aureus), a dangerous bacterium. Known to cause a variety of infections, S. aureus can lead to pneumonia, damage to heart valves resulting in heart failure, and, if it gets into the blood, sepsis, a potentially life-threatening condition. An important cause of infection in hospitals and communities worldwide, the MRSA strain of this bacterium is notorious for its ability to become resistant to antibiotics. Significantly, therefore, there are currently no vaccines available for the prevention of S. aureus infections.
While S. aureus is carried in around 30 percent of healthy people without causing harm, it is also one of the most dangerous bacterial pathogens. The ability of this bacterium to cause disease is associated with its high efficacy to colonize, spread within the host, and evade the immune system. S. aureus produces numerous pro-virulent factors, including a group of polypeptides (long chains of amino acids) that are capable of damaging the membrane of host cells.
Alpha-hemolysin (Hla), one of the toxins produced by S. aureus, is particularly harmful as it forms pores in cell membranes, resulting in cell damage and tissue injury. The new Dr. Rath Research Institute study therefore focuses on identifying cellular mechanisms via which TF3 can inhibit the harmful effects of this toxin.
Published in the European Journal of Microbiology and Immunology, the study uses computer models and simulations to understand how TF3 interacts with Hla at the molecular level. The scientists found that TF3 directly binds to a specific part of Hla known as the ‘stem’ domain. This binding affects the structure of the stem region, an important factor towards limiting Hla’s damaging activity.
The interaction between TF3 and Hla was found to involve hydrogen bonds and hydrophobic interactions with specific amino acids in the Hla protein. Understanding these interactions is critical for inhibiting the toxic actions of Hla.
In addition to revealing the possible mechanism via which TF3 can inhibit the Hla toxin, the Dr. Rath Research Institute’s concurrent in vitro and animal studies have confirmed the efficacy of this black tea compound in decreasing the activity of the Hla toxin. Through its ability to affect the production and secretion of important factors promoting inflammation, TF3 can alleviate the immune response triggered by Hla. It additionally provides significant protection to the body’s skin barrier and thus can potentially be seen as a beneficial compound for alleviating skin injury.
The new study highlights the fact that other natural compounds, such as myricetin, curcumin, and apigenin, have previously been shown to inhibit Hla activity by targeting the stem region of the toxin. These findings suggest that, in addition to TF3, compounds with a similar structure could be developed into effective agents for preventing the harmful effects of Hla and, by extension, S. aureus infections.
Along with the scientists’ earlier work in this area, this latest Dr. Rath Research Institute study further confirms the health benefits of natural compounds and, by targeting the toxic activity of Hla on multiple levels, could potentially lead to the development of innovative, more effective treatments for S. aureus infections.