You might have heard about lyme disease being transmitted by ticks, but did you know that it is caused by a bacterium that can infect your brain and other parts of the body? The bacteria in question is named Borrelia burgdorferi. By entering a type of brain cell called neuroglia, these bacteria can evade immune surveillance and resist antibiotics.
Antibiotics are often the first line of defense against bacteria. The fact that B. burgdorferi is resistant to these drugs means that researchers must find a new way to combat lyme disease. Dr. Robert Gilmore and coworkers decided to investigate how B. burgdorferi enters human cells. They reasoned that they could use this new knowledge to block bacterial entry into cells, rendering the bacteria more susceptible to antibiotics and the immune system.
Gilmore’s group discovered that B. burgdorferitake advantage of a process called “coiling phagocytosis” to enter human cells. Phagocytosis occurs when cells extend bits of their cytoplasm to engulf material in their environment. Coiling phagocytosis specifically describes the process whereby bits of cytoplasm coil intricately around external material and capture it. Gilmore and colleagues also discovered that during the entry process the human protein Daam1 interacts with a Borrelia lipoprotein (think protein with fats attached) known as BBA66 that coats the bacteria.
This study provides important new clues about how B. burgdorferi enters human cells. A better understanding of bacterial internalization pathways like coiling phagocytosis may aid the development of targeted therapeutics that could kill drug-resistant bacteria.
Summary written by: Matthew Curry
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Human neuroglial cells internalize Borrelia burgdorferi by coiling phagocytosis mediated by Daam1
Shanna K. Williams, Zachary P. Weiner, Robert D. Gilmore
