15 February 2018

Leo Joosten, theme Infectious diseases and global health, and colleagues published in PNAS about the role of glutathione metabolism in host defense against Borrelia burdorferi infection.

Publication: link.

Borrelia burgdorferi, the bacterium that causes Lyme disease, has a very limited metabolism of its own and therefore relies heavily on the host for the supply of nutrients. This study describes that during this process, the bacterium also alters cellular metabolism in the host. Specifically, it was found that when human white blood cells were exposed to B. burgdorferi, the levels of the important antioxidant glutathione increased around  10-fold. Surprisingly, this appeared to have limited effect on the oxidative state of the cell. Instead, glutathione was found to be a critical regulator of B. burgdorferi-induced cytokine production, likely through the process of protein glutathionylation.

Importantly, this study finds that glutathione metabolism is also altered in patients with Lyme disease, even weeks to months after the initial infection. This suggests that these metabolic alterations may persist even after the bacterium has been cleared.

Taken together, this study not only provide more insight into the pathogenesis of Lyme disease, but also underlines how host-pathogen interactions in metabolism can play crucial roles in host defense against pathogens.

Leo Joosten


 

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