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Bacteria Take Cover in Lymph Nodes

Bacteria Take Cover in Lymph Nodes

"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, 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 Borrelia burgdorferi have apparently struck an intricate balance that allows the bacteria to both provoke and elude the animal's immune response."

Lyme disease, the most important tick-borne disease in the United States is caused by Borrelia burgdorferi, corkscrew-shaped bacteria also known as spirochetes. The disease is transmitted to humans and animals through bites from infected deer ticks.

They found that when mice were infected with Borrelia 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 Borrelia 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 Borrelia 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 Borrelia 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."



MEDICA.de; Source: University of California - Davis

 
 
 

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