Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum

In visceral leishmaniasis (VL) endemic areas, a minority of infected individuals progress to disease since most of them develop protective immunity. Therefore, we investigated the risk markers of VL within nonimmune sector. Analyzing infected symptomatic and, asymptomatic, and noninfected individual...

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Main Authors: Márcia Dias Teixeira Carvalho, Diego Peres Alonso, Célia Maria Vieira Vendrame, Dorcas Lamounier Costa, Carlos Henrique Nery Costa, Guilherme Loureiro Werneck, Paulo Eduardo Martins Ribolla, Hiro Goto
Format: Article
Language:English
Published: Wiley 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/230129
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author Márcia Dias Teixeira Carvalho
Diego Peres Alonso
Célia Maria Vieira Vendrame
Dorcas Lamounier Costa
Carlos Henrique Nery Costa
Guilherme Loureiro Werneck
Paulo Eduardo Martins Ribolla
Hiro Goto
author_facet Márcia Dias Teixeira Carvalho
Diego Peres Alonso
Célia Maria Vieira Vendrame
Dorcas Lamounier Costa
Carlos Henrique Nery Costa
Guilherme Loureiro Werneck
Paulo Eduardo Martins Ribolla
Hiro Goto
author_sort Márcia Dias Teixeira Carvalho
collection DOAJ
description In visceral leishmaniasis (VL) endemic areas, a minority of infected individuals progress to disease since most of them develop protective immunity. Therefore, we investigated the risk markers of VL within nonimmune sector. Analyzing infected symptomatic and, asymptomatic, and noninfected individuals, VL patients presented with reduced high-density lipoprotein cholesterol (HDL-C), elevated triacylglycerol (TAG), and elevated very-low-density lipoprotein cholesterol (VLDL-C) levels. A polymorphism analysis of the lipoprotein lipase (LPL) gene using HindIII restriction digestion (N = 156 samples) (H+ = the presence and H− = the absence of mutation) revealed an increased adjusted odds ratio (OR) of VL versus noninfected individuals when the H+/H+ was compared with the H−/H− genotype (OR = 21.3; 95% CI = 2.32–3335.3; P = 0.003). The H+/H+ genotype and the H+ allele were associated with elevated VLDL-C and TAG levels (P < 0.05) and reduced HDL-C levels (P < 0.05). An analysis of the L162V polymorphism in the peroxisome proliferator-activated receptor alpha (PPARα) gene (n = 248) revealed an increased adjusted OR when the Leu/Val was compared with the Leu/Leu genotype (OR = 8.77; 95% CI = 1.41–78.70; P = 0.014). High TAG (P = 0.021) and VLDL-C (P = 0.023) levels were associated with susceptibility to VL, whereas low HDL (P = 0.006) levels with resistance to infection. The mutated LPL and the PPARα Leu/Val genotypes may be considered risk markers for the development of VL.
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spelling doaj-art-0f8563dc30a34b4e990a32ea0a7b625b2025-02-03T05:50:29ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/230129230129Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantumMárcia Dias Teixeira Carvalho0Diego Peres Alonso1Célia Maria Vieira Vendrame2Dorcas Lamounier Costa3Carlos Henrique Nery Costa4Guilherme Loureiro Werneck5Paulo Eduardo Martins Ribolla6Hiro Goto7Laboratório de Soroepidemiologia e Imunobiologia, Instituto de Medicina Tropical de São Paulo, Universidade de São Paulo, Avenida Dr. Enéas de Carvalho Aguiar 470, Prédio II, 4° Andar, 05403-000 São Paulo, SP, BrazilDepartamento de Parasitologia, Instituto de Biociências, Universidade Estadual Paulista, 18618-970 Botucatu, SP, BrazilLaboratório de Soroepidemiologia e Imunobiologia, Instituto de Medicina Tropical de São Paulo, Universidade de São Paulo, Avenida Dr. Enéas de Carvalho Aguiar 470, Prédio II, 4° Andar, 05403-000 São Paulo, SP, BrazilInstituto de Doenças Tropicais Natan Portella, Universidade Federal do Piauí, 64001-450 Teresina, PI, BrazilInstituto de Doenças Tropicais Natan Portella, Universidade Federal do Piauí, 64001-450 Teresina, PI, BrazilDepartamento de Epidemiologia, Instituto de Medicina Social, Universidade do Estado do Rio de Janeiro, 20550-900 Rio de Janeiro, RJ, BrazilDepartamento de Parasitologia, Instituto de Biociências, Universidade Estadual Paulista, 18618-970 Botucatu, SP, BrazilLaboratório de Soroepidemiologia e Imunobiologia, Instituto de Medicina Tropical de São Paulo, Universidade de São Paulo, Avenida Dr. Enéas de Carvalho Aguiar 470, Prédio II, 4° Andar, 05403-000 São Paulo, SP, BrazilIn visceral leishmaniasis (VL) endemic areas, a minority of infected individuals progress to disease since most of them develop protective immunity. Therefore, we investigated the risk markers of VL within nonimmune sector. Analyzing infected symptomatic and, asymptomatic, and noninfected individuals, VL patients presented with reduced high-density lipoprotein cholesterol (HDL-C), elevated triacylglycerol (TAG), and elevated very-low-density lipoprotein cholesterol (VLDL-C) levels. A polymorphism analysis of the lipoprotein lipase (LPL) gene using HindIII restriction digestion (N = 156 samples) (H+ = the presence and H− = the absence of mutation) revealed an increased adjusted odds ratio (OR) of VL versus noninfected individuals when the H+/H+ was compared with the H−/H− genotype (OR = 21.3; 95% CI = 2.32–3335.3; P = 0.003). The H+/H+ genotype and the H+ allele were associated with elevated VLDL-C and TAG levels (P < 0.05) and reduced HDL-C levels (P < 0.05). An analysis of the L162V polymorphism in the peroxisome proliferator-activated receptor alpha (PPARα) gene (n = 248) revealed an increased adjusted OR when the Leu/Val was compared with the Leu/Leu genotype (OR = 8.77; 95% CI = 1.41–78.70; P = 0.014). High TAG (P = 0.021) and VLDL-C (P = 0.023) levels were associated with susceptibility to VL, whereas low HDL (P = 0.006) levels with resistance to infection. The mutated LPL and the PPARα Leu/Val genotypes may be considered risk markers for the development of VL.http://dx.doi.org/10.1155/2014/230129
spellingShingle Márcia Dias Teixeira Carvalho
Diego Peres Alonso
Célia Maria Vieira Vendrame
Dorcas Lamounier Costa
Carlos Henrique Nery Costa
Guilherme Loureiro Werneck
Paulo Eduardo Martins Ribolla
Hiro Goto
Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum
Mediators of Inflammation
title Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum
title_full Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum
title_fullStr Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum
title_full_unstemmed Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum
title_short Lipoprotein Lipase and PPAR Alpha Gene Polymorphisms, Increased Very-Low-Density Lipoprotein Levels, and Decreased High-Density Lipoprotein Levels as Risk Markers for the Development of Visceral Leishmaniasis by Leishmania infantum
title_sort lipoprotein lipase and ppar alpha gene polymorphisms increased very low density lipoprotein levels and decreased high density lipoprotein levels as risk markers for the development of visceral leishmaniasis by leishmania infantum
url http://dx.doi.org/10.1155/2014/230129
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