Role of cholesterol in parasitic infections

Bansal, Devendra; Bhatti, Harinderpal Singh; Sehgal, Rakesh

doi:10.1186/1476-511x-4-10

Cited by 104 publications

(65 citation statements)

References 62 publications

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“…Increasing evidence suggests that host lipids are manipulated by, and allocated to pathogens. Helminths may regulate host lipid metabolism by stimulating a decrease in total cholesterol levels [107], particularly low-density lipoprotein (LDL) and Apolipoprotein B [132]. Several mechanisms may account for these decreases.…”

Section: Cardio-metabolic Protective Effects Of Helminth Infectionmentioning

confidence: 99%

“…Helminths and protozoans (e.g. giardia) cannot synthesize their own lipids, and so consume and metabolize host lipids to generate phospholipid membranes [132], exploiting the host lipidome for their own survival and reproduction [84, 134, 135]. Other pathogens, including bacteria such as H. pylori and M. tuberculosis also exploit host lipids for their own growth, maintenance and signaling [136].…”

Section: Cardio-metabolic Protective Effects Of Helminth Infectionmentioning

confidence: 99%

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Cardiovascular disease and type 2 diabetes in evolutionary perspective: A critical role for helminths?

Gurven

Trumble

Stieglitz

et al. 2016

EMPH

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Heart disease and type 2 diabetes are commonly believed to be rare among contemporary subsistence-level human populations, and by extension prehistoric populations. Although some caveats remain, evidence shows these diseases to be unusual among well-studied hunter-gatherers and other subsistence populations with minimal access to healthcare. Here we expand on a relatively new proposal for why these and other populations may not show major signs of these diseases. Chronic infections, especially helminths, may offer protection against heart disease and diabetes through direct and indirect pathways. As part of a strategy to insure their own survival and reproduction, helminths exert multiple cardio-protective effects on their host through their effects on immune function and blood lipid metabolism. Helminths consume blood lipids and glucose, alter lipid metabolism, and modulate immune function towards Th-2 polarization—which combined can lower blood cholesterol, reduce obesity, increase insulin sensitivity, decrease atheroma progression, and reduce likelihood of atherosclerotic plaque rupture. Traditional cardiometabolic risk factors, coupled with the mismatch between our evolved immune systems and modern, hygienic environments may interact in complex ways. In this review, we survey existing studies in the non-human animal and human literature, highlight unresolved questions and suggest future directions to explore the role of helminths in the etiology of cardio-metabolic disease.

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Section: Cardio-metabolic Protective Effects Of Helminth Infectionmentioning

confidence: 99%

Section: Cardio-metabolic Protective Effects Of Helminth Infectionmentioning

confidence: 99%

Cardiovascular disease and type 2 diabetes in evolutionary perspective: A critical role for helminths?

Gurven

Trumble

Stieglitz

et al. 2016

EMPH

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“…In addition to its role in providing energy for various physiological processes, lipid metabolism has been implicated in infectious and parasitic diseases (19). Lipid carrier proteins have been reported to reduce the toxicity of lipopolysaccharide in both invertebrates (20,21) and mammals (22,23).…”

Section: Lipophorin (Lp)mentioning

confidence: 99%

Regulation of Lipid Metabolism Genes, Lipid Carrier Protein Lipophorin, and Its Receptor during Immune Challenge in the Mosquito Aedes aegypti

Cheon

Shin

Bian

et al. 2006

Journal of Biological Chemistry

109

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In the mosquito Aedes aegypti, the expression of two fat body genes involved in lipid metabolism, a lipid carrier protein lipophorin (Lp) and its lipophorin receptor (LpRfb), was significantly increased after infections with Gram (؉) bacteria and fungi, but not with Gram (؊) bacteria. The expression of these genes was enhanced after the infection with Plasmodium gallinaceum. RNA interference (RNAi) knockdown of Lp strongly restricted the development of Plasmodium oocysts, reducing their number by 90%. In Vg-⌬REL1-A transgenic mosquitoes, with gain-of-function phenotype of Toll/REL1 immune pathway activated after blood feeding, both the Lp and LpRfb genes were overexpressed independently of septic injury. The same phenotype was observed in the mosquitoes with RNAi knockdown of Cactus, an IB inhibitor in the Toll/REL1 pathway. These results showed that, in the mosquito fat body, both Lp and LpRfb gene expression were regulated by the Toll/REL1 pathway during immune induction by pathogen and parasite infections. Indeed, the proximal region of the LpRfb promoter contained closely linked binding motifs for GATA and NF-B transcription factors. Transfection and in vivo RNAi knockdown experiments showed that the bindings of both GATA and NF-B transcription factors to the corresponding motif were required for the induction of the LpRfb gene. These findings suggest that lipid metabolism is involved in the mosquito systemic immune responses to pathogens and parasites. Lipophorin (Lp)2 is the major lipid carrier protein in insects. It delivers lipids to various organs via the hemolymph as a reusable shuttle, with no concomitant degradation of the protein matrix of the Lp particle. The fat body, which is an insect analog of vertebrate liver and adipose tissue combined, plays a key role in lipid metabolism by being the site of lipid storage and mobilization. The loading and unloading of lipids into and from fat body cells is accomplished by a shuttle mechanism involving Lp and a multiprotein complex called a lipid transfer particle. The lipophorin particle consists of three apolipoproteins: apolipoprotein I, apolipoprotein II, and apolipoprotein III (1-3). ApoLpI and apoLpII are encoded by a single gene (4 -6). Likewise, mosquito Aedes aegypti Lp consists of apoLpI and apoLpII, the mRNAs of which originate from a single large precursor RNA, indicating that they are encoded by the same gene. Aedes Lp protein level increases upon ingestion of a blood meal, when the mosquito needs an increased rate of lipid transport to developing oocytes. Lipophorin in the whole bodies reaches its maximal levels by 40 -48 h post-blood meal (PBM) when major events of egg yolk and lipid deposition have been completed. However, Lp mRNA and the rate of Lp synthesis in the fat body reach their maximal levels at 18 -20 h PBM (7, 8 -10).The intracellular uptake of Lp is mediated by its cognate lipophorin receptor (LpR), which belongs to the superfamily of low density lipoprotein receptors (LDLRs) (11-15). LpRs have been cloned from several insects, in...

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“…Bansal et al 5. reported that most of the parasites induce significant changes in lipid profiles in patients having active infections.…”

Section: Introductionmentioning

confidence: 99%

Hypocholesterolemia in Patients with an Amebic Liver Abscess

Flores¹,

Obregón²,

Tamez³

et al. 2014

Gut Liver

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Background/AimsMany parasites induce changes in the lipid profiles of the host. Cholesterol increases the virulence of Entamoeba histolytica in animal models and in vitro culture. This study aimed to determine, in patients with an amebic liver abscess, the correlation between cholesterol and other features, such as the size and number of abscesses, standard hematological and serum chemistry profiles, liver tests, and duration of hospital stay.MethodsA total of 108 patients with an amebic liver abscess and 140 clinically healthy volunteers were investigated. Cholesterol and triglycerides were measured in the sera. The data from medical observations and laboratory tests were obtained from the clinical records.ResultsA total of 93% of patients with an amebic liver abscess showed hypocholesterolemia not related to any of the studied parameters. Liver function tests correlated with the size of the abscess. The most severe cases of amebic liver disease or death were found in patients whose cholesterol levels continued to decrease despite receiving antiamebic treatment and hospital care.ConclusionsOur results show that the hypocholesterolemia observed in patients with an amebic liver abscess is not related to any of the clinical and laboratory features analyzed. This is the first study relating hypocholesterolemia to severity of hepatic amebiasis.

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Role of cholesterol in parasitic infections

Cited by 104 publications

References 62 publications

Cardiovascular disease and type 2 diabetes in evolutionary perspective: A critical role for helminths?

Cardiovascular disease and type 2 diabetes in evolutionary perspective: A critical role for helminths?

Regulation of Lipid Metabolism Genes, Lipid Carrier Protein Lipophorin, and Its Receptor during Immune Challenge in the Mosquito Aedes aegypti

Hypocholesterolemia in Patients with an Amebic Liver Abscess

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