OSU scientists replace mice genes to study vitamin D’s effects on infections

Eugene, Ore. — Research from Oregon State University has shown a new model suggesting vitamin D treatment can dramatically reduce the quantity of disease-causing bacteria in skin wounds.

OSU scientist Adrian Gombart and his collaborators in the past have examined the vitamin’s role in fighting infection, but in their new study mice were given a human gene that provides a barrier against infections and is promoted by the bioactive form of vitamin D.

Mice naturally have a similar gene, but vitamin D does not trigger it. The scientists replaced the mouse gene, called Camp, with the human gene, called CAMP, which gave the mice increased resistance to gut and staph infections, caused by the bacterium Staphylococcus aureus, when vitamin D was introduced.

“Vitamin D3 regulates the expression of the CAMP, and Staphylococcus aureus is an important human pathogen that causes skin infections,” Gombart said in a news release. “With our mouse model, we showed that treating a skin wound infected with S. aureus with the bioactive form of vitamin D significantly reduced the number of bacteria in the wound.”

Vitamin D, which is fat-soluble and present in very few foods, promotes calcium absorption in the gut and is needed for bone growth. Vitamin D, manufactured by the body when triggered by sunlight, is also important for cell growth, neuromuscular function, and reduction of inflammation.

The scientists believe their new model will be useful as research into vitamin D-induced expression of CAMP progresses, involving diseases caused by microorganisms and also conditions that are “non-pathogenic,” such as inflammatory bowel disease.

The finding, Gombart said, suggests vitamin D can be used to increase protection against infection by increasing CAMP levels. Those findings recently were published in the Journal of Steroid Biochemistry and Molecular Biology.