Hijacking and Use of Host Lipids by Intracellular Pathogens
- Authors: Alvaro Toledo1, Jorge L. Benach2
- Editors: Indira T. Kudva3, John P. Bannantine4
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VIEW AFFILIATIONS HIDE AFFILIATIONSAffiliations: 1: Department of Molecular Genetics and Microbiology, Stony Brook University, Center for Infectious Diseases at the Center for Molecular Medicine, Stony Brook, NY 11794; 2: Department of Molecular Genetics and Microbiology, Stony Brook University, Center for Infectious Diseases at the Center for Molecular Medicine, Stony Brook, NY 11794; 3: National Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, Ames, IA; 4: National Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, Ames, IA
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Received 02 December 2014 Accepted 21 April 2015 Published 21 December 2015
- Correspondence: Jorge L. Benach, [email protected]

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Abstract:
Intracellular bacteria use a number of strategies to survive, grow, multiply, and disseminate within the host. One of the most striking adaptations that intracellular pathogens have developed is the ability to utilize host lipids and their metabolism. Bacteria such as Anaplasma, Chlamydia, or Mycobacterium can use host lipids for different purposes, such as a means of entry through lipid rafts, building blocks for bacteria membrane formation, energy sources, camouflage to avoid the fusion of phagosomes and lysosomes, and dissemination. One of the most extreme examples of lipid exploitation is Mycobacterium, which not only utilizes the host lipid as a carbon and energy source but is also able to reprogram the host lipid metabolism. Likewise, Chlamydia spp. have also developed numerous mechanisms to reprogram lipids onto their intracellular inclusions. Finally, while the ability to exploit host lipids is important in intracellular bacteria, it is not an exclusive trait. Extracellular pathogens, including Helicobacter, Mycoplasma, and Borrelia, can recruit and metabolize host lipids that are important for their growth and survival.
Throughout this chapter we will review how intracellular and extracellular bacterial pathogens utilize host lipids to enter, survive, multiply, and disseminate in the host.
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Citation: Toledo A, Benach J. 2015. Hijacking and Use of Host Lipids by Intracellular Pathogens. Microbiol Spectrum 3(6):VMBF-0001-2014. doi:10.1128/microbiolspec.VMBF-0001-2014.




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References

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Abstract:
Intracellular bacteria use a number of strategies to survive, grow, multiply, and disseminate within the host. One of the most striking adaptations that intracellular pathogens have developed is the ability to utilize host lipids and their metabolism. Bacteria such as Anaplasma, Chlamydia, or Mycobacterium can use host lipids for different purposes, such as a means of entry through lipid rafts, building blocks for bacteria membrane formation, energy sources, camouflage to avoid the fusion of phagosomes and lysosomes, and dissemination. One of the most extreme examples of lipid exploitation is Mycobacterium, which not only utilizes the host lipid as a carbon and energy source but is also able to reprogram the host lipid metabolism. Likewise, Chlamydia spp. have also developed numerous mechanisms to reprogram lipids onto their intracellular inclusions. Finally, while the ability to exploit host lipids is important in intracellular bacteria, it is not an exclusive trait. Extracellular pathogens, including Helicobacter, Mycoplasma, and Borrelia, can recruit and metabolize host lipids that are important for their growth and survival.
Throughout this chapter we will review how intracellular and extracellular bacterial pathogens utilize host lipids to enter, survive, multiply, and disseminate in the host.

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Figures
Structure of (A) cholesterol, (B) ceramide, (C) sphingomyelin, (D) phosphatidylcholine, and (E) GM1 ganglioside.

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FIGURE 1
Structure of (A) cholesterol, (B) ceramide, (C) sphingomyelin, (D) phosphatidylcholine, and (E) GM1 ganglioside.
Negative-stain transmission electron microscopy image showing the localization of lipid rafts in Borrelia burgdorferi. Cholesterol glycolipids were detected by an antibody conjugated to 6-nm gold particles. From reference 137 . Bar represents 100 nm.

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FIGURE 2
Negative-stain transmission electron microscopy image showing the localization of lipid rafts in Borrelia burgdorferi. Cholesterol glycolipids were detected by an antibody conjugated to 6-nm gold particles. From reference 137 . Bar represents 100 nm.
Schematic representation of the tricarboxylic acid and methyl citrate cycles. In green, the glyoxylate shunt, a variation of the tricarboxylic acid cycle.

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FIGURE 3
Schematic representation of the tricarboxylic acid and methyl citrate cycles. In green, the glyoxylate shunt, a variation of the tricarboxylic acid cycle.
Tables
Bacterial pathogens that incorporate cholesterol

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TABLE 1
Bacterial pathogens that incorporate cholesterol
Bacteria species that use lipid rafts to enter the host cell

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TABLE 2
Bacteria species that use lipid rafts to enter the host cell
Supplemental Material
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