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K Buffen, M Oosting, S Mennens, PK Anand, TS Plantinga, P Sturm, FL van de Veerdonk, JW van der Meer, RJ Xavier, TD Kannegati, MG Netea and LA Joosten
Abstract
Borrelia burgdorferi sensu lato is the causative agent of Lyme disease (LD). Recent studies have shown that recognition of the spirochete is mediated mainly by TLR2 and NOD2. The latter receptor has been associated with the induction of the intracellular degradation process called autophagy. The present study demonstrated for the first time the induction of autophagy by exposure to B. burgdorferi and that autophagy modulates the B. burgdorferi-dependent cytokine production. Human PBMCs treated with autophagy inhibitors showed an increased IL-1β and IL-6 production in response to the exposure of the spirochete, while TNFα production was unchanged. Autophagy induction against B. burgdorferi was dependent on reactive oxygen species (ROS) since cells from patients with chronic granulomatous disease (CGD), which are defective in ROS production, also produced elevated IL-1β. Further, the enhanced production of the pro-inflammatory cytokines was because of the elevated mRNA expression in the absence of autophagy. Our results thus demonstrate the induction of autophagy, which in-turn modulates cytokine production, by B. burgdorferi for the first time.
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Concepts
Reactive oxygen species, Spirochaete, Spirochaetes, Cytokine, Bacteria, Lyme disease, Borrelia, Borrelia burgdorferi
MeSH headings
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