**4. Conclusion**

*S. aureus* is a major bacterial pathogen that develops resistance to medical antibiotics. It has been reported to cause clinical infections and contamination of a broad variety of foods that may result in foodborne illness. These include canned mushroom, breaded chicken products, cheese, and raw milk as well on handles of shopping carts causing 185 000 cases of foodborne illnesses in the United States each year. *S. aureus* bacteria are present on the skin patients with atopic dermatitis. Many strains of *S. aureus* isolated from atopic skin lesions produce enterotoxins with superantigenic properties. *S. aureus* produces the virulent staphylococcal enterotoxin A, a single chain protein that consists of 233 amino acid residues. It has been estimated that the toxin that is secreted by the bacteria is associated with 78% of staphylococcal outbreaks. Our studies show that naturally occurring edible apple phenolic and olive compounds can both inactivate *S. aureus* bacteria and reduce the biological/toxicological properties of the toxin produced by these bacteria and that the food dye Phloxine B inhibits the release of SEA from the pathogens. Whether these novel approaches have therapeutic potential against atopic dermatitis and other diseases merits further study.

The described studies are part of a broader effort, the specific objective of which is to transform toxic proteins to nontoxic, digestible proteins in foods. For example, apple and other polyphenols present in numerous plant foods such as teas, sweet potatoes, and jujube fruits and seeds contain electron-rich aromatic structures and ionizable phenolic OH groups. These structures can in theory change the toxin via non-covalent binding to the toxin and/or by altering the distribution of ionic charges via H-bonding between OH groups and ionizable groups of the protein. We have no direct evidence for this theory, but note that in molecular simulation studies, we observed multiple hydrogen-bonding interactions between polyphenolic tea catechins and cell membranes that may result in anti-bactericidal effects due to disruption of the cell membranes followed by cell death (Sirk et al., 2009; Sirk et al., 2008; Sirk et al., 2011).
