Hijacking and Use of Host Lipids by Intracellular Pathogens

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.

Host membrane lipids are trafficked to membranes of intravacuolar bacteriumEhrlichia chaffeensis

“…Hijacking and utilization of host lipids are known for intracellular pathogens (reviewed in refs. [56][57][58][59]. For example, the closely related bacteria in the order Rickettsiales, Anaplasma phagocytophilum, hijacks cholesterol from NPC1-mediated LDLcholesterol vesicular trafficking pathways (60)(61)(62).…”

“…The extracellular bacterium Borrelia burgdorferi, the agent of tick-borne Lyme disease, also lacks LPS in its membrane (88). Instead, its membranes contain free cholesterol and cholesterol glycolipids that exist as lipid raft-like microdomains, and the growth of this spirochete requires an external cholesterol source (57,(89)(90)(91). Studies suggested that Borrelia encodes cholesterol modification enzymes to synthesize cholesterol glycolipids (92,93), and Borrelia membrane lipoproteins like OspA and OspB can interact with cholesterol lipids (89,94).…”

Lipid Profiles in Lyme Borreliosis: A Potential Role for Apheresis?

“…Given the evidence that [1] lipids are implicated in the pathogenesis and severity of Lyme disease and its complications [2], and the fact that elevated LDL and triglycerides are a significant risk factor (particularly in combination with inflammation) for cardiovascular disease, and [3] the documented risk of patients with Lyme disease for other atherosclerosis, ischemic strokes and carditis [17,18] and, [4] finally, the role of cardiometabolic disturbances, including obesity and dyslipidemia, may suppress innate immunity and allow neuroborreliosis [19,20]. These data clearly justify the need for further studies providing individualized and effective treatment for this patient group.…”

“…Borrelia bacteria recruit and metabolize host lipids that are essential for their growth and survival [1]. Therefore, Lyme disease caused by Borrelia burgdorferi requires cholesterol for survival of the microbe in vivo.…”

Determinants of Raft Partitioning of the Helicobacter pylori Pore-Forming Toxin VacA

“…Many bacterial protein toxins, including VacA, are thought to utilize lipid rafts as the first step in the intoxication of host cells (27). To provide a direct measure of VacA's association with rafts, as well as to define features of the protein that mediate its affinity for raft versus nonraft domains, we analyzed VacA's phase preference using GPMVs.…”