Cell Host & Microbe
Volume 19, Issue 6, 8 June 2016, Pages 837-848
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Article
Trypanosoma brucei Parasites Occupy and Functionally Adapt to the Adipose Tissue in Mice

https://doi.org/10.1016/j.chom.2016.05.002Get rights and content
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Highlights

  • T. brucei parasites accumulate in the adipose tissue early after mouse infection

  • Adipose tissue forms (ATFs) can replicate and are capable of infecting naive mice

  • ATFs are transcriptionally distinct and upregulate genes for fatty acid metabolism

  • ATFs can actively uptake exogenous myristate and form β-oxidation intermediates

Summary

Trypanosoma brucei is an extracellular parasite that causes sleeping sickness. In mammalian hosts, trypanosomes are thought to exist in two major niches: early in infection, they populate the blood; later, they breach the blood-brain barrier. Working with a well-established mouse model, we discovered that adipose tissue constitutes a third major reservoir for T. brucei. Parasites from adipose tissue, here termed adipose tissue forms (ATFs), can replicate and were capable of infecting a naive animal. ATFs were transcriptionally distinct from bloodstream forms, and the genes upregulated included putative fatty acid β-oxidation enzymes. Consistent with this, ATFs were able to utilize exogenous myristate and form β-oxidation intermediates, suggesting that ATF parasites can use fatty acids as an external carbon source. These findings identify the adipose tissue as a niche for T. brucei during its mammalian life cycle and could potentially explain the weight loss associated with sleeping sickness.

Keywords

African trypanosomes
fat
mouse infection
fatty acid β-oxidation
metabolism
transcriptome

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