Erythritol Availability in Bovine, Murine and Human Models Highlights a Potential Role for the Host Aldose Reductase during Brucella Infection

Erythritol is the preferential carbon source for most brucellae, a group of facultative intracellular bacteria that cause a worldwide zoonosis. Since this polyol is abundant in genital organs of ruminants and swine, it is widely accepted that erythritol accounts at least in part for the characterist...

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Veröffentlicht in:Frontiers in microbiology 2017-06, Vol.8, p.1088-1088
Hauptverfasser: Barbier, Thibault, Machelart, Arnaud, Zúñiga-Ripa, Amaia, Plovier, Hubert, Hougardy, Charlotte, Lobet, Elodie, Willemart, Kevin, Muraille, Eric, De Bolle, Xavier, Van Schaftingen, Emile, Moriyón, Ignacio, Letesson, Jean-Jacques
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Sprache:eng
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Zusammenfassung:Erythritol is the preferential carbon source for most brucellae, a group of facultative intracellular bacteria that cause a worldwide zoonosis. Since this polyol is abundant in genital organs of ruminants and swine, it is widely accepted that erythritol accounts at least in part for the characteristic genital tropism of brucellae. Nevertheless, proof of erythritol availability and essentiality during intracellular multiplication has remained elusive. To investigate this relationship, we compared Δ (erythritol-sensitive and thus predicted to be attenuated if erythritol is present), Δ (erythritol-tolerant but showing reduced growth if erythritol is a crucial nutrient) and wild type in various infection models. This reporting system indicated that erythritol was available but not required for multiplication in bovine trophoblasts. However, mice and humans have been considered to lack erythritol, and we found that it was available but not required for multiplication in human and murine trophoblastic and macrophage-like cells, and in mouse spleen and conceptus (fetus, placenta and envelopes). Using this animal model, we found that infected cells and tissues contained aldose reductase, an enzyme that can account for the production of erythritol from pentose cycle precursors.
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2017.01088