4.7 Article

Trypanosoma brucei Parasites Occupy and Functionally Adapt to the Adipose Tissue in Mice

Journal

CELL HOST & MICROBE
Volume 19, Issue 6, Pages 837-848

Publisher

CELL PRESS
DOI: 10.1016/j.chom.2016.05.002

Keywords

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Funding

  1. HHMI [55007419]
  2. EMBO [2151]
  3. FCT [SFRH/BPD/89833/2012, SFRH/BD/51286/2010, SFRH/BD/80718/2011]
  4. Wellcome Trust [093228]
  5. MRC [MR/M020118/1]
  6. European Community [602773]
  7. Belspo [PAI 7/41]
  8. ERC-NANOSYM
  9. Fundação para a Ciência e a Tecnologia [SFRH/BD/51286/2010, SFRH/BD/80718/2011] Funding Source: FCT
  10. Medical Research Council [MR/M020118/1] Funding Source: researchfish
  11. MRC [MR/M020118/1] Funding Source: UKRI

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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 beta-oxidation enzymes. Consistent with this, ATFs were able to utilize exogenous myristate and form beta-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.

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