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 byLeishmania infantum

Author:

Carvalho Márcia Dias Teixeira1,Alonso Diego Peres2,Vendrame Célia Maria Vieira1,Costa Dorcas Lamounier3,Costa Carlos Henrique Nery3,Werneck Guilherme Loureiro45,Ribolla Paulo Eduardo Martins2,Goto Hiro16ORCID

Affiliation:

1. Laboratório 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, Brazil

2. Departamento de Parasitologia, Instituto de Biociências, Universidade Estadual Paulista, 18618-970 Botucatu, SP, Brazil

3. Instituto de Doenças Tropicais Natan Portella, Universidade Federal do Piauí, 64001-450 Teresina, PI, Brazil

4. Departamento de Epidemiologia, Instituto de Medicina Social, Universidade do Estado do Rio de Janeiro, 20550-900 Rio de Janeiro, RJ, Brazil

5. Instituto de Estudos em Saúde Coletiva, Universidade Federal do Rio de Janeiro, 21941-598 Rio de Janeiro, RJ, Brazil

6. Departamento de Medicina Preventiva, Faculdade de Medicina, Universidade de São Paulo, 01246-903 São Paulo, SP, Brazil

Abstract

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.

Funder

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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