期刊
CELL HOST & MICROBE
卷 19, 期 6, 页码 837-848出版社
CELL PRESS
DOI: 10.1016/j.chom.2016.05.002
关键词
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资金
- HHMI [55007419]
- EMBO [2151]
- FCT [SFRH/BPD/89833/2012, SFRH/BD/51286/2010, SFRH/BD/80718/2011]
- Wellcome Trust [093228]
- MRC [MR/M020118/1]
- European Community [602773]
- Belspo [PAI 7/41]
- ERC-NANOSYM
- Fundação para a Ciência e a Tecnologia [SFRH/BD/51286/2010, SFRH/BD/80718/2011] Funding Source: FCT
- Medical Research Council [MR/M020118/1] Funding Source: researchfish
- MRC [MR/M020118/1] Funding Source: UKRI
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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