Lyme Disease Receptor Identified in Tick Guts
November 12, 2004
Source: Yale University
Researchers at Yale School of Medicine have identified a Lyme disease receptor called TROSPA that is used by disease agents to invade ticks. Lyme disease, the most common tick-borne disease in the United States, is caused by spirochete bacteria Borrelia burgdorferi, which also cause arthritis in humans.
The purpose of the study, published November 12 in the journal Cell, was to identify how Lyme disease pathogens survive inside ticks. "We identified a receptor inside the tick gut that the spirochete bacteria use to colonize or invade ticks," said principal investigator Erol Fikrig, M.D., professor of internal medicine/rheumatology and in the Section of Microbial Pathogenesis, and Department of Epidemiology and Public Health at Yale School of Medicine. "When we eliminated or blocked the receptor in the ticks, they were no longer able to carry the Lyme disease agent Borellia burgforferi." "This opens up potential new avenues to disrupt the Borellia's life cycle and offers strategies for improving diagnosis and treatment of Lyme disease," Fikrig added.
To characterize the Lyme disease receptor, the team cloned the gene for the receptor from ticks. After they expressed the purified receptor gene, they showed that the Lyme disease agent Borellia burgforferi binds to the receptor. "When we blocked the receptors with antibodies or when we used RNA interference to knock the receptor out of the ticks, they no longer carried Borellia burgforferi," said Fikrig. "We are excited to learn more about the life cycle of this important pathogen," Fikrig added. "This information can also be used to study other vector-borne diseases such as West Nile virus and Malaria," Fikrig added.
Other authors on the study included Utpal Pal, Xin Li, Tian Wang, Ruth R. Montgomery, Nandhini Ramamoorthi, Aravinda M. deSilva, Fukai Bao, Xiaofeng Yang, Marc Pypaert, Deepti Pradhan, Fred S. Kantor, Sam Telford and John F. Anderson. Citation: Cell, No. 19 Volume 4, November 12, 2004.