Abstract
Lipids are a broad group of molecules required for cell maintenance and homeostasis. Various intracellular pathogens have developed mechanisms of modulating and sequestering host lipid processes for a large array of functions for both bacterial and host cell survival. Among the host cell lipid functions that intracellular bacteria exploit for infection are the modulation of host plasma membrane microdomains (lipid rafts) required for efficient bacterial entry; the recruitment of specific lipids for membrane integrity of intracellular vacuoles; and the utilization of host lipid droplets for the regulation of immune responses and for energy production through fatty acid β-oxidation and oxidative phosphorylation. The majority of published studies on the utilization of these host lipid pathways during infection have focused on intracellular bacterial pathogens that reside within a vacuole during infection and, thus, have vastly different requirements for host lipid metabolites when compared to those intracellular pathogens that are released into the host cytosol upon infection. Here we summarize the mechanisms by which intracellular bacteria sequester host lipid species and compare the modulation of host lipid pathways and metabolites during host cell infection by intracellular pathogens residing in either a vacuole or within the cytosol of infected mammalian cells. This review will also highlight common and unique host pathways necessary for intracellular bacterial growth that could potentially be targeted for therapeutic intervention.
Highlights
Lipids are broadly described as hydrophobic or amphipathic molecules that are involved in various biological functions including mediating immune signaling, regulating vesicle trafficking, providing energy storage and production, and structural membrane composition [1,2,3,4,5,6,7,8,9,10]
Some studies have demonstrated that Rickettsia spp. stimulate an increase in prostaglandin production during in vivo and in vitro infection models indicating that these mechanisms discussed could be used for the production of lipid immune modulators derived from host lipid droplets (LDs) as described for C. pneumoniae, C. burnetii, and M. leprae [170,171,172] (Figure 2)
F. tularensis infection are still unknown. Both obligate and facultative intracellular bacteria have developed several strategies to regulate and manipulate host processes for efficient intracellular growth. Among these is the modulation of host lipid metabolism that has been demonstrated to be required for the maintenance of host cell homeostasis and to be implemented in various intracellular infections for increased persistence and disease progression
Summary
Lipids are broadly described as hydrophobic or amphipathic molecules that are involved in various biological functions including mediating immune signaling, regulating vesicle trafficking, providing energy storage and production, and structural membrane composition [1,2,3,4,5,6,7,8,9,10]. Intracellular pathogens modify host lipid composition by regulating host cell uptake of exogenous lipids from the environment and modulating the expression of enzymes involved in the host de novo lipid biosynthetic pathways [12,13,14,15,16] This alteration in host lipid composition can be beneficial to the pathogen by providing a number of different functions including: (i) Employing storage and/or free lipids for energy production. Lipid organization within host membranes play an important role in the regulation of signaling pathways by creating “hot spots,” known as lipid rafts, for enabling the association of receptors with external and internal stimuli These functional, highly organized membrane regions are utilized by various intracellular bacterial pathogens for entry into the host cell [18]. The research discussed highlights differences in vacuolar and cytosolic bacteria’s use of host lipids for pathogen membrane structure, host LD alterations during infection, and lipid utilization for energy production
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