In this article on the MicrobiologyBytes blog, the author discusses how certain bacteria use sphingomyelins from their hosts in order to create their own lipids:
"Fifteen years ago, in a series of elegant studies, Hackstadt and colleagues showed that the obligate intracellular bacteria Chlamydia trachomatis save on their lipid needs by incorporating sphingomyelins (SMs) made by their host. Shortly after, Hatch and McClarty’s teams reported that several eukaryotic glycerophospholipids are also trafficked from the host to the bacteria, which replace host-synthesized straight-chain fatty acids by their own branched-chain fatty acids. Even cholesterol, a lipid rarely found in bacteria, was shown to accumulate in Chlamydia. As a result of this intense exploitation of host lipids, the composition of the bacterial membrane is closer to that of a eukaryotic cell than to that of a prokaryote.So this got me thinking about Borrelia, too, as Borrelia burgdorferi contains free cholesterol and cholesterol glycolipids. Cholesterol 6-O-acyl-β-D-galactopyranoside and its non-acylated form are significant components of membranes of the spirochete Borrelia burgdorferi.
Throughout their developmental cycle, chlamydiae reside within a membrane-bounded compartment, the inclusion. How they acquire host lipids remains an open question. Possible mechanisms studied so far involve vesicular trafficking from host compartments, including vesicular traffic out of the Golgi apparatus, fusion with multivesicular body–derived vesicles, and engulfment of lipid droplets."
Rerouting of Host Lipids by Bacteria: Are You CERTain You Need a Vesicle? (2011) PLoS Pathog 7(9): e1002208. doi:10.1371/journal.ppat.1002208
Then there is this research which was brought to my attention:
Macrophages infected with Mycobacterium tuberculosis (M.tb) are known to be refractory to IFN-a stimulation. Previous studies have shown that M.tb express components such as the 19-kDa lipoprotein and peptidoglycan that can bind to macrophage receptors including the Toll-like receptor 2 resulting in the loss in IFN-a responsiveness. However, it is unclear whether this effect is limited to infected macrophages. We have previously shown that M.tb-infected macrophages release exosomes which are 30-100 nm membrane bound vesicles of endosomal origin that function in intercellular communication. These exosomes contain mycobacterial components including the 19-kDa lipoprotein and therefore we hypothesized that macrophages exposed to exosomes may show limited response to IFN-a stimulation.Similar to what happens with Mycobacterium tuberculosis, Borrelia burgdorferi engages in blebbing, where vesicles form on the surface of the bacteria and are released. Each vesicle or "bleb" has been shown to contain lipoproteins, and some research has indicated these vesicles are not just an artifact or sign of cellular injury.
Gram-negative bacteria vesicles can contain various virulence factors such as toxins, proteases, adhesins, and lipopolysaccharide, which are utilized to establish a colonization niche, modulate host defense and response, and impair host cell function.
Some bacteria may selectively create vesicles with specific lipoproteins, such as Porphyromonas gingivalis - but in this bacteria, lipopolysaccarides (LPS) are thought to do the sorting. But Borrelia burgdorferi does not have LPS, so some other mechanism determines which lipoproteins are contained in vesicles.
In earlier research it was shown that not only do Borrelia burgdorferi create vesicles which contain outer membrane proteins and lipids - but they also have been shown to contain DNase I-resistant plasmid DNa - suggesting they were at least partially derived from the inner membrane.
So, now that I've pointed out these things, what am I wondering?
If like Chlamydia trachomatis, Borrelia burgdorferi also has a membrane that is more like a eukaryotic membrane? If so, can this contribute to its stealthy nature?
How much Borrelia burgdorferi really relies on its host for its own needs? Compared to other bacteria, Bb has a relatively small genome and is an obligate mostly-extracellular parasite, which means it needs to take what it needs from its host in order to survive. How does it build these lipid rafts and attach to endothelial cells?
If Borrelia burgdorferi creates vesicles or these blebs which contain a mix of outer surface lipids and proteins as well as some inner membrane components, is it possible that it leaves a trail of antigenic material behind it and moves into new areas undetected because its membrane does not produce the same immunological response that blebs or vesicles do?
Somewhat Related Trivia: Chikungunya virus can hide from the immune system inside apoptotic blebs. You think something is now innocuous and on its way out? Think again - these blebs carry the virus through the blood stream to other cells. This virus also manages to replicate inside macrophages while not causing any inflammatory effect. This is a reminder that Borrelia burgdorferi is not the only pathogen that does interesting and stealthy things!
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