By Maureen McArthur

"Our work has focused on how the bacteria regulate proteins found on their surface, allowing the bacteria to escape immune defenses."

-- Brian Stevenson,
UK College of Medicine researcher.

Feb. 5, 2002 (Lexington, Ky.) -- A study led by a University of Kentucky College of Medicine researcher Brian Stevenson has revealed how Borrelia burgdorferi, corkscrew-shaped bacteria that cause Lyme disease, escapes the immune defenses of many different hosts.

The study appears in the Feb.1 issue of Infection and Immunity. Transmitted to humans through tick bites, the bacteria were discovered only about 20 years ago (although descriptions of a rash associated with tick bites date back to the early 1900s).

However, the bacteria can live in a wide range of animals, which suggests the bacteria can evade the immune defenses of many different hosts.

"Our work has focused on how the bacteria regulate proteins found on their surface, allowing the bacteria to escape immune defenses," said Stevenson, assistant professor, Department of Microbiology, Immunology and Molecular Genetics.

Stevenson has found that the bacteria can "hide" from proteins called complement, a key component of the immune defense. These complement proteins puncture the cell membranes of invading microorganisms or mark them for destruction by other parts of the immune system.

Proteins on the surface of B. burgdorferi, called Erp, bind to an inhibitor in the host that inactivates complement proteins. This prevents complement from doing damage to the bacteria. Different Erp proteins can bind inhibitors from different hosts, enabling the bacteria to infect many animals, including humans.

Stevenson currently is examining the mechanisms of interactions between Erp proteins and complement inhibitors, and how Erp synthesis is regulated as the bacteria infect humans.