The bacteria that cause Lyme disease, one of the most important emerging diseases in the United States, appear to hide out in the lymph nodes, triggering a significant immune response, but one that is not strong enough to rout the infection, according to a new report by researchers at the University of California, Davis
Results from this groundbreaking study involving mice may explain why some people experience repeated infections of Lyme disease. The study appears online in the journal Public Library of Science Pathogens.
“Our findings suggest for the first time that Borrelia burgdorferi, the bacteria that cause Lyme disease in people, dogs and wildlife, have developed a novel strategy for subverting the immune response of the animals they infect,” said Professor Nicole Baumgarth, an authority on immune responses at the UC Davis Center for Comparative Medicine.
“At first it seems counter intuitive that an infectious organism would choose to migrate to the lymph nodes where it would automatically trigger an immune response in the host animal,” Baumgarth said. “But B. burgdorferi have apparently struck an intricate balance that allows the bacteria to both provoke and elude the animal’s immune response.”
“Science Daily” recently reported these findings, and yet so many medical experts still maintain that there is no such thing as chronic Lyme disease. As each year passes and studies continue to pile up proving the personal testimonies of hundreds of thousands of suffering victims. Thanks to U.C.Davis we have more concrete proof.
Swollen lymph nodes, or lymphadenopathy, is one of the hallmarks of Lyme disease, although it has been unclear why this occurs or how it affects the course of the disease. The UC Davis research team set out to explore in mice the mechanisms that cause the enlarged lymph nodes and to determine the nature of the resulting immune response.
They found that when mice were infected with B. burgdorferi, these live spirochetes accumulated in the animals’ lymph nodes. The lymph nodes responded with a strong, rapid accumulation of B cells, white blood cells that produce antibodies to fight infections. Also, the presence of B. burgdorferi caused the destruction of the distinct architecture of the lymph node that usually helps it to function normally.
While B cells accumulated in large numbers and made some specific antibodies against B. burgdorferi, they did not form “germinal centers,” structures that are needed for the generation of highly functional and long-lived antibody responses.
“Overall, these findings suggest that B. burgdorferi hinder the immune system from generating a response that is fully functional and that can persist and protect after repeat infections,” Baumgarth said. “Thus, the study might explain why people living in endemic areas can be repeatedly infected with these disease-causing spirochetes.”
In addition to Baumgarth, members of the UC Davis research team include Stephen Barthold, director of the Center for Comparative Medicine; Emir Hodzic, director of the Real-Time PCR Research and Diagnostics Core Facility; staff scientist Sunlian Feng; graduate student Christine Hastey; and Stefan Tunev, formerly of the Center for Comparative Medicine and now at Medtronic Inc.
University of California – Davis (2011, June 17). Lyme disease bacteria take cover in lymph nodes. ScienceDaily. Retrieved June 21, 2011, from http://www.sciencedaily.com /releases/2011/06/110616193911.htm
Stefan S. Tunev, Christine J. Hastey, Emir Hodzic, Sunlian Feng, Stephen W. Barthold, Nicole Baumgarth. Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation. PLoS Pathogens, 2011; 7 (5): e1002066 DOI: 10.1371/journal.ppat.1002066