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Review
. 2017 Dec 7;13(12):e1006669.
doi: 10.1371/journal.ppat.1006669. eCollection 2017 Dec.

Pathogen manipulation of host metabolism: A common strategy for immune evasion

Zachary Freyberg  1   2 , Eric T Harvill  3   4
Affiliations
Review

Pathogen manipulation of host metabolism: A common strategy for immune evasion

Zachary Freyberg et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Model of pathogen interactions between host metabolism and immune response.
We propose a generalizable model demonstrating the means by which pathogens manipulate host metabolism to facilitate infection. Diverse pathogens, including P. falciparum and B. pertussis, decrease host blood glucose levels. This results in an impaired host immune response that consequently exacerbates and/or prolongs infection by providing the pathogen with improved opportunities to increase load and/or persistence and enhance transmission to other hosts.
Fig 2
Fig 2. Model for PTX- and ACT-induced hyperinsulinemia.
Following infection, B. pertussis produces PTX, which acts not only within the respiratory tract but also directly on insulin-secreting pancreatic beta cells. Within these cells, PTX inhibits Gαi/o signaling that ordinarily inhibits adenylate cyclase, the enzyme responsible for cAMP synthesis. This leads to increases in cAMP and activates PKA, a key stimulator of insulin release. In parallel, B. pertussis also secretes ACT, which directly increases cAMP levels to also produce hyperinsulinemia and subsequent hypoglycemia in the host. ACT, adenylate cyclase toxin; PKA, protein kinase A; PTX, pertussis toxin.
See this image and copyright information in PMC

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