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Leishmania amazonensis

ABSTRACT: Iron uptake controls the generation of Leishmania infective forms through regulation of ROS levels .

PROVIDER: PRJNA177795 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR594631.fastq.gz	Fastqsanger.gz
	SRR594632.fastq.gz	Fastqsanger.gz
	SRR594633.fastq.gz	Fastqsanger.gz
	SRR594634.fastq.gz	Fastqsanger.gz

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Similar Datasets

Leishmania amazonensis

Project description:Iron uptake controls the generation of Leishmania infective forms through regulation of ROS levels .

| PRJNA177795 | ENA

Iron uptake controls the generation of Leishmania infective forms through regulation of ROS levels .

Project description:During its life cycle Leishmania undergoes extreme environmental changes, alternating between insect vectors and vertebrate hosts. In mammals the parasites replicate within parasitophorous vacuoles of macrophages, compartments that contain low concentrations of iron. Here we show that stimulation of iron transport, which is induced in Leishmania amazonensis by an iron-poor environment, triggers the differentiation of avirulent promastigotes into virulent amastigotes. Iron depletion from the culture medium triggered expression of the LIT1 ferrous iron transporter, growth arrest, and differentiation of wild type promastigotes into infective amastigotes. In contrast, LIT1 null promastigotes showed continued exponential growth in iron-poor media, followed by massive cell death. Iron depletion from the medium and LIT1 upregulation increased iron superoxide dismutase activity (FeSOD) in wild type, but not in LIT1 null parasites. Notably, the superoxide-generating drug menadione or H2O2 were sufficient to trigger differentiation of wild type promastigotes into fully infective amastigotes. On the other hand, LIT1 null promastigotes accumulated superoxide radical and initiated amastigote differentiation after exposure to H2O2, but not to menadione. Our results reveal a novel role for FeSOD activity and reactive oxygen species (ROS) in orchestrating the differentiation of Leishmania infective stages, in a process regulated by iron availability.

2012-12-15 | GSE41641 | GEO

Iron uptake controls the generation of Leishmania infective forms through regulation of ROS levels .

2012-12-15 | E-GEOD-41641 | biostudies-arrayexpress

Leishmania amazonensis strain:IFLA/BR/67/PH8

Project description:Leishmania iron response

| PRJNA244311 | ENA

Leishmania amazonensis

Project description:Leishmania amazonensis Transcriptome or Gene expression

| PRJNA292915 | ENA

Leishmania amazonensis

Project description:GENE EXPRESSION PROFILING AND MOLECULAR CHARACTERIZATION OF ANTIMONY RESISTANCE IN Leishmania amazonensis

| PRJNA135277 | ENA

Profiling of 2'-O-methylation in Leishmania amazonensis rRNA using RibOxi-seq

Project description:In this study we report the complete repertoire of 2'-O-methylation sites present in the rRNA of Leishmania amazonensis rRNAs and a subset of small RNAs using RibOxi-seq.

2024-05-01 | GSE186879 | GEO

Leishmania TORC1 links nutrient availability to differentiation into infective

Project description:Leishmania TORC1 links nutrient availability to differentiation into infective

2022-10-31 | MSV000090621 | MassIVE

Leishmania major modulates autophagy in host macrophages during intracellular differentiation

Project description:Autophagy generally participates in innate immunity by elimination of intracellular pathogens. However, many of them developed successful strategies to counteract their autolysosomal digestion and lastly to exploit this catabolic cellular process. Protozoan parasites of the genus Leishmania are the causative agent of leishmaniasis, one of the 13 most important tropical diseases. Leishmania persists as endo-parasite in host macrophages, where it uses multiple strategies to manipulate the microbicidal host cell functions and to escape from the host immune system. Understanding how Leishmania interacts with host macrophages during uptake, differentiation, intracellular replication, and release might be the key to develop new drugs in target-directed approaches to treat patient with leishmaniasis. Here, we generated expression profiles from bone marrow-derived macrophages (BMDM) at 1h and 24h post infection (p.i.) with Leishmania major and respective controls.

2015-08-03 | E-GEOD-52624 | biostudies-arrayexpress

Leishmania major infection-induced changes in the small RNA transcriptome of host macrophages.

Project description:Protozoan parasites of the genus Leishmania are the causative agent of leishmaniasis, one of the 13 most important tropical diseases. Leishmania persists as endo-parasite in host macrophages, where it uses multiple strategies to manipulate the microbicidal host cell functions and to escape from the host immune system. Understanding how Leishmania interacts with host macrophages during uptake, differentiation, intracellular replication, and release might be the key to develop new drugs in target-directed approaches to treat patient with leishmaniasis. Short non-coding RNAs are known to regulate the expression of protein-coding genes at post-transcriptional level. Characterization of these processes during Leishmania infection provides deeper insight in the interaction between host and parasites. Here, we generated miRNA expression profiles from bone marrow-derived macrophages (BMDM) at 4h and 24h post infection (p.i.) with Leishmania major and respective controls.

2015-08-03 | E-GEOD-58369 | biostudies-arrayexpress

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