Endosomal signaling by Lyme disease bacterium

What is it about?

Borrelia burgdorferi is the bacterial agent of most cases of Lyme disease in North America and parts of Europe. B. burgdorferi is an extracellular pathogen (i.e., it does not live within mammalian cells). When B. burgdorferi is deposited into the skin by an infected tick during feeding, the spirochete encounters host immune cells that attempt to eliminate the invading bacterium by ingesting (phagocytosing) it. In this manuscript, we demonstrate that B. burgdorferi, although it does not survive inside the cell, nevertheless activates signaling pathways from within the endosome/phagosome that result in the production of type I interferon. Type I IFN, so named because it has been found to 'interfere' with viral replication, confers protection against infections by viruses and certain intracellular bacteria. This manuscript therefore describes an innate immune mechanism that may contribute to Lyme disease pathogenesis and is the first study to identify specific phagosomal receptors involved in type I IFN induction by B. burgdorferi.

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