ArticleInfection and immunity2011
Sphingolipid degradation by Leishmania major is required for its resistance to acidic pH in the mammalian host.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- VAPA mediates lipid exchange between Leishmania amazonensis and host macrophages.PLoS pathogens · 2025Article
- Expanded Proteomic Survey of the Human Parasite Leishmania major Focusing on Changes in Null Mutants of the Golgi GDP-Mannose/Fucose/Arabinopyranose TransporterMicrobiology spectrum · 2022Article
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- Activity of Chitosan and Its Derivatives against Leishmania major and Leishmania mexicanaAntimicrobial agents and chemotherapy · 2020Article
- Article
- Article
- Sterol methyltransferase is required for optimal mitochondrial function and virulence in Leishmania major.Molecular microbiology · 2019Article
- Sphingolipids and Redox Signaling in Renal Regulation and Chronic Kidney Diseases.Antioxidants & redox signaling · 2018Article
- Cyclopropane fatty acid synthesis affects cell shape and acid resistance in Leishmania mexicana.International journal for parasitology · 2018Article
- Plasmenylethanolamine synthesis in Leishmania major.Molecular microbiology · 2016Article
- Simultaneous transcriptional profiling of Leishmania major and its murine macrophage host cell reveals insights into host-pathogen interactions.BMC genomics · 2015Article
- Sterol biosynthesis is required for heat resistance but not extracellular survival in leishmania.PLoS pathogens · 2014Article
- Sphingosine kinase A is a pleiotropic and essential enzyme for Leishmania survival and virulence.Molecular microbiology · 2013Article
- Parasite-derived arginase influences secondary anti-Leishmania immunity by regulating programmed cell death-1-mediated CD4+ T cell exhaustion.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Leishmania parasites possess a platelet-activating factor acetylhydrolase important for virulence.Molecular and biochemical parasitology · 2012Article
- Article
- Sphingolipid degradation in Leishmania (Leishmania) amazonensis.PLoS neglected tropical diseases · 2012Article
- Subversion and Utilization of Host Innate Defense by Leishmania amazonensis.Frontiers in immunology · 2012Article
- Sphingolipid and ceramide homeostasis: potential therapeutic targets.Biochemistry research international · 2012Article
- Endocytosis and Sphingolipid Scavenging in Leishmania mexicana Amastigotes.Biochemistry research international · 2012Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Leishmania parasites alternate between flagellated promastigotes in sand flies and nonflagellated amastigotes in mammals, causing a spectrum of serious diseases. To survive, they must resist the harsh conditions in phagocytes (including acidic pH, elevated temperature, and increased oxidative/nitrosative stress) and evade the immune response. Recent studies have highlighted the importance of sphingolipid (SL) metabolism in Leishmania virulence. In particular, we have generated a Leishmania major iscl(-) mutant which is deficient in SL degradation but grows normally as promastigotes in culture. Importantly, iscl(-) mutants cannot induce pathology in either immunocompetent or immunodeficient mice yet are able to persist at low levels. In this study, we investigated how the degradation of SLs might contribute to Leishmania infection. First, unlike wild-type (WT) L. major, iscl(-) mutants do not trigger polarized T cell responses in mice. Second, like WT parasites, iscl(-) mutants possess the ability to downregulate macrophage activation by suppressing the production of interleukin-12 (IL-12) and nitric oxide. Third, during the stationary phase, iscl(-) promastigotes were extremely vulnerable to acidic pH but not to other adverse conditions, such as elevated temperature and oxidative/nitrosative stress. In addition, inhibition of phagosomal acidification significantly improved iscl(-) survival in murine macrophages. Together, these findings indicate that SL degradation by Leishmania is essential for its adaption to the acidic environment in phagolysosomes but is not required for the suppression of host cell activation. Finally, our studies with iscl(-) mutant-infected mice suggest that having viable, persistent parasites is not sufficient to provide immunity against virulent Leishmania challenge.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.