<i>Ehrlichia chaffeensis</i>
            and
            <i>Anaplasma phagocytophilum</i>
            Lack Genes for Lipid A Biosynthesis and Incorporate Cholesterol for Their Survival

Lin, Mingqun; Rikihisa, Yasuko

doi:10.1128/iai.71.9.5324-5331.2003

Cited by 248 publications

(235 citation statements)

References 42 publications

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“…Ehrlichiosis is known as a catabolic disease -like most haemoparasites, the agent of the disease cannot synthesize its own lipids -and is predominantly bound to HDL derived from the host's plasma (20,22). In a present study, HDL values were significantly lower in both groups infected with vector-borne diseases compared to healthy dogs.…”

Section: Co-infected (N = 23)supporting

confidence: 48%

“…Moreover, a defect in the removal of triglycerides from circulation, or increased hepatic production, may be associated with the increase (25). Bacteria incorporate the cholesterol derived from host cells to support membrane integrity; therefore, cholesterol has become necessary for their survival and infection (22). Nevertheless, the production or biosynthetic modification of cholesterol enzymes was not identified in E. canis.…”

Section: Co-infected (N = 23)mentioning

confidence: 98%

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Oxidative status and lipid profile in mono- and co-infection with canine monocytic ehrlichiosis

Gültekin

Ural

Paşa

et al. 2017

Medycyna Weterynaryjna

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SummaryVector-borne diseases in dogs are a major health problem of zoonotic importance. Canine monocytic ehrlichiosis (CME) is one of the most common vector-borne infections in dogs. Co-infections with vectorborne diseases are reported to cause more severe pathological effects than mono-infections. The current study investigates the effects of mono-and co-infections with CME on oxidative status and lipid profiles in dogs. Dogs with vector-borne diseases were divided into two groups, mono-infected (n = 22) and co-infected (n = 23) with CME, and compared to a healthy group (n = 20). Double and triple co-infections with other vector-borne diseases included A. phagocytophilum, L. infantum, and D. immitis. The serum lipid profile (high-density lipoprotein (HDL), low-density lipoprotein (LDL), cholesterol, and triglycerides) and the total and individual markers of oxidative status (total antioxidant capacity (TAC), total oxidant status (TOS), malondialdehyde (MDA), paraoxonase (PON-1), and arylesterase (ARE)) were evaluated. Significant decreases in PON-1 and ARE enzyme activities and HDL concentration, as well as increases in TOS level, MDA, LDL, and triglyceride concentrations were determined in both mono-and co-infected groups compared to the healthy control group. No significant differences between the groups were found in the TAC level or cholesterol concentration. In conclusion, alterations in lipid profile and increase in oxidative stress were observed in dogs with CME compared to the healthy control group, however, no significant differences were detected between mono-and co-infected dogs.

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Section: Co-infected (N = 23)supporting

confidence: 48%

Section: Co-infected (N = 23)mentioning

confidence: 98%

Oxidative status and lipid profile in mono- and co-infection with canine monocytic ehrlichiosis

Gültekin

Ural

Paşa

et al. 2017

Medycyna Weterynaryjna

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“…This is particularly pertinent because A. phagocytophilum is technically categorized as a Gram-negative organism. However, unique physical characteristics and previously determined molecular evidence suggest the absence of peptidoglycan from A. phagocytophilum (62)(63)(64), which would nullify any effect IAFGP (or P1) would have on A. phagocytophilum. Our earlier work described the role for elevated levels of IAFGP, upon A. phagocytophilum infection of Ixodes ticks, to protect ticks from the cold environment (26).…”

Section: Discussionmentioning

confidence: 99%

Pathogen-mediated manipulation of arthropod microbiota to promote infection

Abraham

Liu

Jutras

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

227

295

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Arthropods transmit diverse infectious agents; however, the ways microbes influence their vector to enhance colonization are poorly understood.Ixodes scapularisticks harbor numerous human pathogens, includingAnaplasma phagocytophilum,the agent of human granulocytic anaplasmosis. We now demonstrate thatA. phagocytophilummodifies theI. scapularismicrobiota to more efficiently infect the tick.A. phagocytophiluminduces ticks to expressIxodes scapularisantifreeze glycoprotein (iafgp), which encodes a protein with several properties, including the ability to alter bacterial biofilm formation. IAFGP thereby perturbs the tick gut microbiota, which influences the integrity of the peritrophic matrix and gut barrier—critical obstacles forAnaplasmacolonization. Mechanistically, IAFGP binds the terminald-alanine residue of the pentapeptide chain of bacterial peptidoglycan, resulting in altered permeability and the capacity of bacteria to form biofilms. These data elucidate the molecular mechanisms by which a human pathogen appropriates an arthropod antibacterial protein to alter the gut microbiota and more effectively colonize the vector.

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“…They also have noncholesterol glycolipids, monogalactosyl-diacylglycerol in B. burgdorferi and monoglucosyl-diacylglycerol in relapsing-fever Borrelia, as well as many lipoproteins (7)(8)(9)(10)(11)(12)(13)(14)(15). The presence of cholesterol is not common among prokaryotes, but it is increasingly being reported in bacterial pathogens other than Borrelia spp., including species of Helicobacter, Mycoplasma, Ehrlichia, Anaplasma, and Brachyspira (16)(17)(18)(19)(20).…”

mentioning

confidence: 99%

Hypercholesterolemia and ApoE deficiency result in severe infection with Lyme disease and relapsing-fever Borrelia

Toledo¹,

Monzón²,

Coleman

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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The Lyme disease (Borrelia burgdorferi) and relapsing-fever (Borrelia hispanica) agents have distinct infection courses, but both require cholesterol for growth. They acquire cholesterol from the environment and process it to form cholesterol glycolipids that are incorporated onto their membranes. To determine whether higher levels of serum cholesterol could enhance the organ burdens of B. burgdorferi and the spirochetemia of B. hispanica in laboratory mice, apolipoprotein E (apoE)-deficient and low-density lipoprotein receptor (LDLR)-deficient mice that produce large amounts of serum cholesterol were infected with both spirochetes. Both apoE-and LDLR-deficient mice infected with B. burgdorferi had an increased number of spirochetes in the joints and inflamed ankles compared with the infected wild-type (WT) mice, suggesting that mutations in cholesterol transport that result in high serum cholesterol levels can affect the pathogenicity of B. burgdorferi. In contrast, elevated serum cholesterol did not lead to an increase in the spirochetemia of B. hispanica. In the LDLR-deficient mice, the course of infection was indistinguishable from the WT mice. However, infection of apoE-deficient mice with B. hispanica resulted in a longer spirochetemia and increased mortality. Together, these results argue for the apoE deficiency, and not hypercholesterolemia, as the cause for the increased severity with B. hispanica. Serum hyperlipidemias are common human diseases that could be a risk factor for increased severity in Lyme disease.cholesterol | Lyme disease | relapsing fever | Borrelia | tick-borne C holesterol is an essential structural component of the cell membrane of vertebrate animals, and it is required for membrane integrity and fluidity. In addition to being a component of the membrane, cholesterol is the precursor of steroid hormones and bile. In eukaryotic cells, cholesterol and sphingolipids are the main components of membrane microdomains known as lipid rafts. These microdomains are characterized as being more tightly packed than the surrounding bilayer and enriched with proteins involved in signaling (1-3).In the bloodstream of humans and other vertebrates, cholesterol is transported in lipoprotein complexes. Apolipoprotein E (apoE) binds cholesterol for transport through the circulatory system as apoE-containing chylomicrons and very-low-density lipoprotein (VLDL) particles. These apoE-cholesterol particles are internalized through the interaction with the low-density lipoprotein receptors (LDLRs). LDLR is one of the cell-surface receptors in cells that binds to apoE to clear the lipoprotein particles from the blood (4). Both apoE-deficient (apoE − ) and LDLR-deficient (LDLR − ) mice show elevated serum cholesterol levels and develop atherosclerotic plaques (5, 6). These mice are the most used mouse models for hyperlipidemia and atherosclerosis research.Lyme disease and relapsing-fever Borrelia have very distinct infection courses and niches in the host. In experimental mouse infections, relapsing-fever borre...

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Ehrlichia chaffeensis and Anaplasma phagocytophilum Lack Genes for Lipid A Biosynthesis and Incorporate Cholesterol for Their Survival

Cited by 248 publications

References 42 publications

Oxidative status and lipid profile in mono- and co-infection with canine monocytic ehrlichiosis

Oxidative status and lipid profile in mono- and co-infection with canine monocytic ehrlichiosis

Pathogen-mediated manipulation of arthropod microbiota to promote infection

Hypercholesterolemia and ApoE deficiency result in severe infection with Lyme disease and relapsing-fever Borrelia

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