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07:36
Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
Published on: May 1, 2015
Filariasis and lymphoedema
K M Pfarr1, A Y Debrah, S Specht
1Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
Parasite Immunology
|October 15, 2009
Summary
Secondary lymphoedema (LE) from filariasis has a genetic basis, with immune responses and vascular endothelial growth factors (VEGF) playing key roles. Identifying genetic risk factors may enable prevention of this debilitating condition.
Area of Science:
- Immunology
- Genetics
- Tropical Medicine
Background:
- Secondary lymphoedema (LE) from filariasis is prevalent, affecting a minority of infected individuals.
- Family clustering suggests a genetic predisposition to developing LE after filarial infection.
- Most infected individuals develop immunosuppression, tolerating parasites, while a subset mounts stronger immune responses.
Purpose of the Study:
- To investigate the immunogenetic basis of lymphoedema development in filariasis.
- To identify genetic risk factors for lymphoedema.
- To understand the role of immune responses and VEGF in lymphoedema pathogenesis.
Main Methods:
- Analysis of immune responses (Th1, Th2, Th17, regulatory T-cells, IgG4) in infected individuals.
- Investigating the role of innate immune responses and vascular endothelial growth factors (VEGF).
- Examining the effect of Wolbachia endosymbiont depletion with doxycycline on VEGF levels.
- Identifying single-nucleotide polymorphisms (SNPs) in VEGF, cytokine, and toll-like receptor (TLR) genes.
Main Results:
- Innate immune responses triggered by filarial antigens activate VEGF, promoting lymph vessel hyperplasia.
- Depletion of Wolbachia using doxycycline reduced plasma VEGF and soluble VEGF-receptor-3 levels.
- SNPs in VEGF, cytokine, and TLR genes show potential functional relevance.
- A VEGF-A SNP associated with lymphangiogenesis is linked to hydrocele, a condition sharing sequelae with LE.
Conclusions:
- Immune responses and VEGF signaling are critical in lymphoedema development.
- Genetic factors, particularly SNPs in immune and VEGF-related genes, contribute to LE susceptibility.
- Identifying these immunogenetic risk factors is crucial for developing preventative strategies against filarial lymphoedema.
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