Altered lipid parameters in patients infected with Entamoeba histolytica, Entamoeba dispar and Giardia lamblia

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

doi:10.1080/09674845.2005.11732686

Cited by 24 publications

(19 citation statements)

References 9 publications

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“…Other authors reported abnormal cephalin-cholesterol flocculation test in patients with ALA and patients with intestinal amebiasis 22,23. Bansal et al 24. found significantly lower levels of lipid profile in ALA patients and cyst passers of E. histolytica or E. dispar , compared with healthy controls.…”

Section: Discussionmentioning

confidence: 97%

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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Section: Discussionmentioning

confidence: 97%

Hypocholesterolemia in Patients with an Amebic Liver Abscess

Flores¹,

Obregón²,

Tamez³

et al. 2014

Gut Liver

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“…First, the most common site of extra-intestinal infection is the liver, an organ rich in cholesterol. Second, patients who are cyst passers have lower levels of serum cholesterol than those with ALA (Bansal et al, 2005). Third, the virulence of laboratory grown amoebae can be maintained by periodic passage through hamster livers (Neal and Vincent, 1956) or by axenic culture in cholesterol-supplemented media (Sharma, 1959; Singh et al, 1971; Das and Ghoshal, 1976; Bos and van de Griend, 1977; Katiyar et al, 1987; Serrano-Luna et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Localisation to lipid rafts correlates with increased function of the Gal/GalNAc lectin in the human protozoan parasite, Entamoeba histolytica

Welter

Goldston

Temesvari

2011

International Journal for Parasitology

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Entamoeba histolytica is the causative agent of dysentery and liver abscess and is prevalent in developing countries. Adhesion to the host is critical to infection and is mediated by amoebic surface receptors. One such receptor, the Gal/GalNAc lectin, binds to galactose or N-acetylgalactosamine residues on host components and consists of heavy (Hgl), light (Lgl) and intermediate subunits. The mechanism by which the lectin assembles into a functional complex is not known. The parasite also relies on cholesterol-rich domains (lipid rafts) for adhesion. Therefore, it is conceivable that rafts regulate the assembly or function of the lectin. To test this, amoebae were loaded with cholesterol and lipid rafts were purified and characterized. Western blotting showed that cholesterol loading resulted in co-compartmentalization of all three subunits in rafts. This co-compartmentalization was accompanied by an increase in the ability of the amoebae to bind to host cells in a galactose-specific manner, suggesting that there is a correlation between location and function of the Gal/GalNAc lectin. Cholesterol loading did not increase the surface levels of the lectin subunits. Therefore, the cholesterol-induced increase in adhesion was not the result of externalization of an internal pool of subunits. A mutant cell line that modestly responded to cholesterol with a slight increase in adhesion exhibited only a slight enrichment of Hgl and Lgl in rafts. This supports the connection between location and function of the Gal/GalNAc lectin. Actin can also influence the interaction of proteins with rafts. Therefore, the sub-membrane distribution of the lectin subunits was also assessed after treatment with an actin depolymerizing agent, cytochalasin D (CytoD). CytoD-treatment had no effect on the submembrane distribution of the subunits, suggesting that actin does not prevent the association of lectin subunits with rafts in this system. Together, these data provide insight into the molecular mechanisms regulating the location and function of this adhesin.

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“…The result showed significant lower levels of lipid profile [total cholesterol, HDL & LDL] in E. histolytica and E. dispar cyst passers and ALA patients as compared to healthy controls. Also, cyst passers had lower levels of cholesterol than ALA cases [29]. …”

Section: Anaerobic Parasitesmentioning

confidence: 99%

“…Previously, we have reported that receptor Ck dependent signaling is responsible for the regulation of Giardia encystations process by cholesterol [39]. Recently we have observed that patients infected with G. lamblia showed lower levels of lipid parameters (total cholesterol, HDLc and LDLc) as compared to control healthy group [29]. …”

Section: Anaerobic Parasitesmentioning

confidence: 99%

Role of cholesterol in parasitic infections

2005

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The requirement of cholesterol for internalization of eukaryotic pathogens like protozoa (Leishmaniasis, Malaria and Toxoplasmosis) and the exchange of cholesterol along with other metabolites during reproduction in Schistosomes (helminths) under variable circumstances are poorly understood. In patients infected with some other helminthes, alterations in the lipid profile have been observed. Also, the mechanisms involved in lipid changes especially in membrane proteins related to parasite infections remain uncertain. Present review of literature shows that parasites induce significant changes in lipid parameters, as has been shown in the in vitro study where substitution of serum by lipid/cholesterol in medium and in experimental models (in vivo). Thus changes in lipid profile occur in patients having active infections with most of the parasites. Membrane proteins are probably involved in such reactions. All parasites may be metabolising cholesterol, but the exact relationship with pathogenic mechanism is not clear. So far, studies suggest that there may be some factors or enzymes, which allow the parasite to breakup and consume lipid/cholesterol. Further studies are needed for better understanding of the mechanisms involved in vivo. The present review analysis the various studies till date and the role of cholesterol in pathogenesis of different parasitic infections.

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Altered lipid parameters in patients infected with Entamoeba histolytica, Entamoeba dispar and Giardia lamblia

Cited by 24 publications

References 9 publications

Hypocholesterolemia in Patients with an Amebic Liver Abscess

Hypocholesterolemia in Patients with an Amebic Liver Abscess

Localisation to lipid rafts correlates with increased function of the Gal/GalNAc lectin in the human protozoan parasite, Entamoeba histolytica

Role of cholesterol in parasitic infections

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