Advanced search
Start date
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

Full text
Teixeira Carvalho, Marcia Dias [1] ; Alonso, Diego Peres [2] ; Vieira Vendrame, Celia Maria [1] ; Costa, Dorcas Lamounier [3] ; Nery Costa, Carlos Henrique [3] ; Werneck, Guilherme Loureiro [4, 5] ; Martins Ribolla, Paulo Eduardo [2] ; Goto, Hiro [1, 6]
Total Authors: 8
[1] Univ Sao Paulo, Inst Med Trop Sao Paulo, Lab Soroepidemiol & Imunobiol, BR-05403000 Sao Paulo - Brazil
[2] Univ Estadual Paulista, Inst Biociencias, Dept Parasitol, BR-18618970 Botucatu, SP - Brazil
[3] Univ Fed Piaui, Inst Doencas Trop Natan Portella, BR-64001450 Teresina, PI - Brazil
[4] Univ Estado Rio de Janeiro, Inst Social Med, Dept Epidemiol, BR-20550900 Rio De Janeiro, RJ - Brazil
[5] Univ Fed Rio de Janeiro, Inst Estudos Saude Colet, BR-21941598 Rio De Janeiro, RJ - Brazil
[6] Univ Sao Paulo, Fac Med, Dept Prevent Med, BR-01246903 Rio De Janeiro, RJ - Brazil
Total Affiliations: 6
Document type: Journal article
Source: Mediators of Inflammation; 2014.
Web of Science Citations: 6

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 (PPAR alpha) 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 PPAR alpha Leu/Val genotypes may be considered risk markers for the development of VL. (AU)