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Cell Host Microbe. 2016 Jun 8;19(6):837-48. doi: 10.1016/j.chom.2016.05.002. Epub 2016 May 26.

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

Author information

1
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1990-375 Lisboa, Portugal.
2
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1990-375 Lisboa, Portugal; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA; Graduate Program in Areas of Basic and Applied Biology, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4099-002 Porto, Portugal.
3
Biomedical Sciences Research Complex, University of St Andrews, North Haugh, St Andrews, Fife KY16 9ST, UK.
4
Department of Biomedical Sciences, Unit of Veterinary Protozoology, Institute of Tropical Medicine Antwerp, B-2000 Antwerp, Belgium; Department of Physiology, Laboratory of Zoophysiology, University of Ghent, B-9000 Ghent, Belgium.
5
Theoretical Division, Los Alamos National Laboratory, Los Alamos, NM 87545, USA; Guest Professor, Faculdade de Medicina, Universidade de Lisboa, 1990-375 Lisboa, Portugal.
6
Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1990-375 Lisboa, Portugal. Electronic address: lmf@medicina.ulisboa.pt.

Abstract

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; fatty acid β-oxidation; metabolism; mouse infection; transcriptome

Comment in

PMID:
27237364
PMCID:
PMC4906371
DOI:
10.1016/j.chom.2016.05.002
[Indexed for MEDLINE]
Free PMC Article

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