Cholesterol and Phospholipid Uptake by Mycoplasmas

Razin, Shmuel; Efrati, Hava; Kutner, Shirley; Rottem, Shlomo

doi:10.1093/clinids/4.supplement_1.s85

Cited by 19 publications

(18 citation statements)

References 33 publications

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“…This process may in fact aid the mycoplasmas in acquisition of cholesterol, possibly by cleavage of HDL by mycoplasmal cholesterol esterases (31). In this regard, the presence of a protease-sensitive receptor for serum lipoproteins on the surface of the mycoplasmas described earlier might have relevance because this receptor was not present on the surface of the related, but sterol nonrequiring acholeplasmas (2). It remains to be determined whether our observations are specific for M. arthritidis, specific for cholesterolrequiring mycoplasmas, or whether shed bioactive lipopeptides from other organisms can also bind to apoA-1.…”

Section: Discussionmentioning

confidence: 75%

“…As a result, they parasitize the cells of their hosts, acquiring needed nutrients. They lack a rigid cell wall and instead are bound by a triple-layered membrane that maintains structural integrity by incorporating cholesterol derived from high-density lipoprotein (HDL) 3 or low-density lipoprotein (LDL) (1,2). Thus, optimal in vitro culture requires complex medium with serum added as a source of cholesterol and other nutrients.…”

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confidence: 99%

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A Microbial TLR2 Agonist Imparts Macrophage-Activating Ability to Apolipoprotein A-1

Hasebe

Pennock

et al. 2006

The Journal of Immunology

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There is increasing epidemiologic evidence implying a role for chronic infection in atherosclerosis and that microbial TLR agonists may contribute to this disease. Mycoplasma arthritidis is an agent of acute and chronic inflammatory disease in rodents, and has been used extensively as a model for defining the mechanisms involved in arthritis and other inflammatory diseases. We have purified a 28-kDa, apolipoprotein A-1 (apoA-1)-like TLR2-dependent macrophage-activating moiety from a culture of a virulent strain of M. arthritidis. ApoA-1 similarly isolated from uninoculated mycoplasma medium was without bioactivity. The activity of the mycoplasma-derived molecule was resistant to heat and to digestion with proteinase K, but was susceptible to alkaline hydrolysis and H2O2 oxidation. Infrared profiles of normal apoA-1 and that derived from mycoplasma were distinct. Unlike the activity of other mycoplasmal TLR2 agonists such as macrophage-activating lipopeptide-2, activity of the M. arthritidis-derived 28-kDa component was dependent upon CD14, a coreceptor for LPS. Finally, we showed that bioactive lipopeptides prepared from M. arthritidis grown in serum-free medium and also from a 41-kDa known bioactive lipoprotein of M. arthritidis, avidly bound to purified apoA-1 that separated out by SDS-PAGE, induced TNF-α and IL-12p40 both in vitro and in vivo. ApoA-1 is a key functional component of the high-density lipoprotein cholesterol complex by scavenging and removing unwanted lipids. Our finding that this molecule can acquire macrophage-activating properties from microbial TLR2-dependent agonists suggests a novel mechanism whereby some microbial agents might reverse the protective role of apoA-1, thus contributing to the genesis of atherosclerosis.

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Section: Discussionmentioning

confidence: 75%

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confidence: 99%

A Microbial TLR2 Agonist Imparts Macrophage-Activating Ability to Apolipoprotein A-1

Hasebe

Pennock

et al. 2006

The Journal of Immunology

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“…The distribution of lipids in the membrane also appears to be in segregated domains, reminiscent of lipid rafts in Mycoplasma gallisepticum (129). The uptake of cholesterol and phospholipids by several species of Mycoplasma is mediated by protein receptors, presumably for lipoproteins, and also by direct binding to membrane phospholipids and by existing glycolipids as well (130). The lipids of Mycoplasma are involved in cell fusion.…”

Section: Bacterial Use Of Host Lipids For Intracellular Growthmentioning

confidence: 99%

Hijacking and Use of Host Lipids by Intracellular Pathogens

Toledo

Benach

2015

Microbiol Spectr

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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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“…In contrast, HS is much richer in esterified cholesterol than in free cholesterol (5). Razin and his coworkers (3,4,7) reported that mycoplasmas incorporate more free cholesterol than esterified cholesterol into their plasma membranes during growth in a serum-containing medium. Therefore, the high content of phospholipids and free cholesterol in EY may be favorable M. pneumoniae M. pulmonis for the growth of M. pneumoniae.…”

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confidence: 99%