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. 2012 Sep;8(9):e1002887.
doi: 10.1371/journal.ppat.1002887. Epub 2012 Sep 20.

Copper at the front line of the host-pathogen battle

Richard A Festa  1 , Dennis J Thiele
Affiliations

Copper at the front line of the host-pathogen battle

Richard A Festa et al. PLoS Pathog. 2012 Sep.
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Delivery of Cu from the macrophage to the pathogen.
Ctr1 is induced upon activation of the macrophage, possibly leading to increased Cu uptake by the macrophage. Similarly, ATP7A expression is increased and the protein is re-localized to the phagosomal membrane, with the net effect being an increased concentration of Cu in the phagolysosomal lumen. Cu can synergistically react with other effectors such as the production of ROS and NO to promote more oxidative damage. Pathogenic bacteria handle Cu-toxicity mostly through sensing and export mechanisms, while some bacteria have buffering capabilities by binding Cu in chaperones and metallothioneins. Pathogenic fungi, on the other hand, have a higher requirement for Cu usage, but still maintain robust mechanisms for Cu detoxification.
See this image and copyright information in PMC

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