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Alterations in lipoprotein density classes in infantile visceral leishmaniasis: presence of apolipoprotein SAA
E D Bekaert1, E Dole, D Y Dubois
1Unité de Recherches sur les Dyslipidémies et l'Athérosclérose, Hôpital Henri Mondor, Créteil, France.
Insights
Visceral Leishmaniasis in children significantly alters plasma lipoproteins, increasing triglycerides and apolipoprotein E while decreasing HDL cholesterol and other apolipoproteins. These changes may stem from altered immune function or hepatic synthesis during infection.
Area of Science:
- Biochemistry
- Immunology
- Pediatrics
Background:
- Visceral Leishmaniasis (VL) is a severe parasitic disease affecting young children.
- Lipoprotein alterations are common in infectious diseases but poorly understood in pediatric VL.
- Understanding these changes is crucial for managing VL complications.
Purpose of the Study:
- To investigate plasma lipoprotein and apolipoprotein profiles in Tunisian children with active visceral Leishmaniasis.
- To identify specific lipoprotein abnormalities associated with VL.
- To explore potential mechanisms underlying these metabolic changes.
Main Methods:
- Analysis of plasma lipid profiles, including triglycerides and cholesterol levels.
- Quantitative determination of plasma apolipoproteins (A-I, A-II, E, SAA).
- Two-dimensional electrophoresis and immunochemical analysis to identify lipoprotein subspecies (LP-E, LP-SAA).
- Electron microscopy to assess HDL heterogeneity.
Main Results:
- Marked hypertriglyceridaemia and reduced HDL-cholesterol observed in VL patients.
- Significantly decreased levels of apolipoproteins A-I and A-II, with a marked increase in apolipoprotein E.
- Detection of apolipoprotein serum amyloid A (SAA) isoforms and abnormal LP-E particles in LDL and HDL2.
- Abnormalities in HDL3 structure observed via electron microscopy.
Conclusions:
- Active visceral Leishmaniasis induces profound alterations in lipoprotein metabolism in children.
- Increased hepatic synthesis of apolipoprotein SAA and/or altered immune function are potential contributors.
- These findings highlight the systemic impact of VL on lipid metabolism.
Abstract:
This study describes the alterations in the plasma lipoproteins from nine young Tunisian children with active visceral Leishmaniasis. The plasma lipid profile from affected patients was characterized by a marked hypertriglyceridaemia associated with reduced levels of total and high density lipoprotein (HDL)-cholesterol and a significant increase in the plasma ratio of unesterified to total cholesterol. Quantitative determination of plasma apolipoproteins revealed significantly decreased levels of all measured apolipoproteins, especially of apolipoproteins A-I and A-II, with the exception of apolipoprotein E, the levels of which were markedly increased. Moreover, at least two isoforms of the apolipoprotein serum amyloid A (SAA), an acute phase protein, were detected in all patients' plasma using two-dimensional electrophoresis. Immunochemical evidence was presented that apolipoproteins E and SAA, although both primarily associated with apolipoprotein A- (A-I and A-II) as well as with apolipoprotein B-containing lipoproteins, could occur as LP-E and LP-SAA subspecies, devoid of apolipoproteins A and B. However, it should be pointed out that LP-SAA particles were found in HDL2 from only two patients whereas the abnormal LP-E particles were detected in LDL and HDL2 from all investigated patients. The polydispersity and heterogeneity of patients' HDL3 were assessed by electron microscopy. It was further suggested that the profound changes in the lipoprotein metabolism of these young patients may be due to the increased hepatic synthesis of apolipoprotein SAA and/or to their altered immune function during active visceral Leishmaniasis.