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Leishmania Lifecycle

Serum Lipid Profile, Apolipoprotein E Genotype and Visceral Leishmaniasis Infection in a Northeastern Brazilian Population.

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Leishmania Lifecycle

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  1. Serum Lipid Profile, Apolipoprotein E Genotype and Visceral Leishmaniasis Infection in a Northeastern Brazilian Population Adam P. Simons1, Gloria R. Monteiro2, Nubia N. Pontes2, Taysa M. Feitosa2, Upasna Gaur3, Richard D. Pearson4, Mary E. Wilson3, Selma M. Jeronimo21.University of California-Davis, Sacramento, CA, 2.Federal University of Rio Grande do Norte, Natal, Brazil, 3.University of Iowa, Iowa City, IA, 4.University of Virginia, Charlottesville, VA

  2. Leishmania Lifecycle

  3. Environmental and Host Factors Determine Response to Infection ? • Phenotypes: • No Current Infection (N) • -Antibody Neg. • Acute Illness (VL) • Asymptomatic Infection (DTH+) • -Antibody +/- **Wiki commons

  4. Cholesterol Augments Leishmania Infectivity Rodriguez, Gaur, Wilson 2006

  5. Family Pairs Number of Pairs Sibling-Sibling 692 Parent-Offspring 892 Grandparent-Grandchild 268 Avuncular 414 Cousin 249 Cohort of families in VL endemic Area in Natal, Brazil

  6. Serum Lipids by Phenotype

  7. Cholesterol Level by Phenotype vs. Age

  8. ↓ TC, HDL ↓ ApoA, ApoB, ApoC ↑ TG ↑ ApoE Acute VL Effects: Barral et al (1986) Bekaert et al (1992) Nieto (1992)

  9. Parasitic Infection (leptospirosis) ↓ Total Cholesterol, HDL ↑ TG Bacterial infections: ↓ Total Cholesterol, HDL InflammationDyslipidemia ApoE Dijk et al 1999 ↑ Hepatic TG ↓ Lipoprotein Lipase TNFa ↑ LDL Rec. Expression IL-6 Grunfeld et al 1991 Liberopoulous et al 2004

  10. ApoE Genotype and Leishmaniasis? Source: Jeronimo et al 2007 • 109 families in Natal • Linkage Analysis • Chr 9 (VL) • Chr 15 (DTH+) • Chr 19 (DTH+) Apolipoprotein E Jerónimo Genome-Wide Scan 2007

  11. ApoE Genotype Founders CONTROL FAMILIES VL FAMILIES

  12. Selective Pressure of ApoE Oriá et al (2005) Wiki commons

  13. Future Directions • Large-power study of ApoE genotype • Lipid metabolic pathways in VL recovery • LXR, PPAR, Cholesterol Biosynthesis pathway gene expression across disease process.

  14. Acknowledgments • Mary E. Wilson, University of Iowa • Richard D. Pearson, University of Virginia • Noah Craft, University of California • Edgar Carvalho, UFBA • Cristina Otonis, UFRN • Gloria Monteiro, UFRN • Upasna Gaur, University of Iowa • Selma Jerónimo, UFRN NIH, CNPq and UC Davis for financial support

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