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Published on: July 29, 2021
Sphingolipid degradation in Leishmania (Leishmania) amazonensis
Agiesh Balakrishna Pillai1, Wei Xu, Ou Zhang
1Department of Biological Sciences, Texas Tech University, Lubbock, Texas, United States of America.
Plos Neglected Tropical Diseases
|January 4, 2013
Summary
Sphingolipid degradation by the enzyme LaISCL is crucial for Leishmania amazonensis virulence. Its absence attenuates infection, with outcomes varying based on host genetics, unlike in Leishmania major.
Area of Science:
- Parasitology
- Molecular Biology
- Biochemistry
Background:
- Human leishmaniasis presents diverse symptoms caused by over 20 Leishmania species.
- Sphingolipid degradation is vital for Leishmania (Leishmania) major virulence.
- Leishmania (Leishmania) amazonensis causes South American cutaneous leishmaniasis.
Purpose of the Study:
- Investigate the role of sphingolipid degradation in Leishmania (Leishmania) amazonensis virulence.
- Identify the specific enzyme responsible for sphingolipid turnover in L. amazonensis.
Main Methods:
- Identified the enzyme LaISCL in L. amazonensis, localized to mitochondria.
- Generated and complemented LaISCL null mutants (Laiscl(-)) via gene deletion and add-back.
- Assessed mutant phenotypes in vitro (acidic pH, macrophage survival) and in vivo (murine models).
Main Results:
- LaISCL deletion caused hypersensitivity to acidic pH and reduced survival in macrophages.
- Laiscl(-) mutants showed significantly reduced virulence in C57BL/6 mice but were infective in BALB/c mice.
- Wild-type L. amazonensis caused severe pathology in both mouse strains.
Conclusions:
- A single enzyme, LaISCL, mediates sphingolipid turnover in L. amazonensis.
- LaISCL's expression and properties resemble its L. major ortholog.
- Sphingolipid degradation's role in L. amazonensis virulence differs significantly from L. major, depending on host genetics.
