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Curr Opin Microbiol. 2016 Feb;29:30-6. doi: 10.1016/j.mib.2015.10.002. Epub 2015 Nov 3.

Chewing the fat: lipid metabolism and homeostasis during M. tuberculosis infection.

Author information

1
Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA 01605, USA.
2
Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, MA 01605, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.
3
Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14850, USA. Electronic address: bcv8@cornell.edu.

Abstract

The interplay between Mycobacterium tuberculosis lipid metabolism, the immune response and lipid homeostasis in the host creates a complex and dynamic pathogen-host interaction. Advances in imaging and metabolic analysis techniques indicate that M. tuberculosis preferentially associates with foamy cells and employs multiple physiological systems to utilize exogenously derived fatty-acids and cholesterol. Moreover, novel insights into specific host pathways that control lipid accumulation during infection, such as the PPARĪ³ and LXR transcriptional regulators, have begun to reveal mechanisms by which host immunity alters the bacterial micro-environment. As bacterial lipid metabolism and host lipid regulatory pathways are both important, yet inherently complex, components of active tuberculosis, delineating the heterogeneity in lipid trafficking within disease states remains a major challenge for therapeutic design.

PMID:
26544033
DOI:
10.1016/j.mib.2015.10.002
[Indexed for MEDLINE]

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