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Review
. 2017 Aug 3;13(8):e1006408.
doi: 10.1371/journal.ppat.1006408. eCollection 2017 Aug.

Molecular mechanisms of mucormycosis-The bitter and the sweet

Clara Baldin  1 , Ashraf S Ibrahim  1   2
Affiliations
Review

Molecular mechanisms of mucormycosis-The bitter and the sweet

Clara Baldin et al. PLoS Pathog. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

ASI is a founder of Vitalex Biosciences, a company that is aiming to develop rapid diagnostics and immunotherapy for mucormycosis.

Figures

Fig 1
Fig 1. Diagram depicting the interactions of Mucorales with endothelial cells during hematogenous dissemination/organ seeding and the effect of host factors on these interactions and on the immune response.
(A) Hyperglycemia and ketoacidosis result in liberation of iron from serum-sequestering proteins (e.g., transferrin) via glycosylation and protonation, respectively. (B) Ketone bodies (e.g., β-hydroxy butyrate [BHB]) and free iron negatively affect the immune response to the infection, while sodium bicarbonate (NaHCO3) reverses this negative effect by preventing iron release from transferrin and neutralizing acidity. (C) Surface expression of glucose-regulator protein 78 (GRP78) on endothelial cells is enhanced to cope with the stress elicited by hyperglycemia, free iron, and ketone bodies. (D) Glucose, free iron (transported by the high affinity iron permease [Ftr1p]), and BHB also enhance the expression of fungal cell surface CotH, which results in invasion of the endothelium and augmentation of fungal growth. (E) In deferoxamine-treated hosts, the iron-rich ferrioxamine binds to its fungal receptor (ferrioxamine binding proteins [Fob1/Fob2]) then releases iron via a reductive step prior to feeding invading Mucorales via Ftr1p transportation.
See this image and copyright information in PMC

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