ArticlePloS one2012
Intracellular pathogen Leishmania donovani activates hypoxia inducible factor-1 by dual mechanism for survival advantage within macrophage.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- Parasites as Modulators of Angiogenesis: Implications for Vascular Biology and Pathogenesis.Pathogens (Basel, Switzerland) · 2026Review
- Oxygen and immunity toInfection and immunity · 2025Review
- Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal withJID innovations : skin science from molecules to population health · 2025Article
- HIF-α signaling regulates the macrophage inflammatory response duringFrontiers in immunology · 2025Article
- Regulatory Functions of Hypoxia in Host-Parasite Interactions: A Focus on Enteric, Tissue, and Blood Protozoa.Microorganisms · 2023Review
- Crosstalk between hypoxic cellular micro-environment and the immune system: a potential therapeutic target for infectious diseases.Frontiers in immunology · 2023Article
- T Lymphocyte Exhaustion During Human and Experimental Visceral Leishmaniasis.Frontiers in immunology · 2022Review
- HIF-α Activation Impacts Macrophage Function during MurinePathogens (Basel, Switzerland) · 2021Article
- Highlighting the interplay of microRNAs fromParasitology · 2021Review
- Effects of Visceralising Leishmania on the Spleen, Liver, and Bone Marrow: A Pathophysiological Perspective.Microorganisms · 2021Review
- Hypoxia-Inducible Factor 1 Alpha Is Dispensable for Host Defense of Group B Streptococcus Colonization and Infection.Journal of innate immunity · 2021Article
- Transcription Factors Interplay Orchestrates the Immune-Metabolic Response ofFrontiers in cellular and infection microbiology · 2021Review
- Repurposing bioenergetic modulators against protozoan parasites responsible for tropical diseases.International journal for parasitology. Drugs and drug resistance · 2020Article
- An Attempt to Polarize Human Neutrophils Toward N1 and N2 PhenotypesFrontiers in immunology · 2020Article
- Article
- HIF-1α as a central mediator of cellular resistance to intracellular pathogens.Current opinion in immunology · 2019Review
- The HIF-1α/LC3-II Axis Impacts Fungal Immunity in Human Macrophages.Infection and immunity · 2019Article
- HIF-1α hampers dendritic cell function and Th1 generation during chronic visceral leishmaniasis.Scientific reports · 2018Article
- Hypoxia, Hypoxia-Inducible Factor-1α, and Innate Antileishmanial Immune Responses.Frontiers in immunology · 2018Review
- HIF-1alpha and infectious diseases: a new frontier for the development of new therapies.Revista do Instituto de Medicina Tropical de Sao Paulo · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Recent evidence established a crucial role for mammalian oxygen sensing transcription factor hypoxia inducible factor-1 (HIF-1) in innate immunity against intracellular pathogens. In response to most of these pathogens host phagocytes increase transcription of HIF-1α, the regulatory component of HIF-1 to express various effector molecules against invaders. Leishmania donovani (LD), a protozoan parasite and the causative agent of fatal visceral leishmaniasis resides in macrophages within mammalian host. The mechanism of HIF-1 activation or its role in determining the fate of LD in infected macrophages is still not known. To determine that J774 macrophages were infected with LD and about four-fold increase in HIF-1 activity and HIF-1α expression were detected. A strong increase in HIF-1α expression and nuclear localization was also detected in LD-infected J774 cells, peritoneal macrophages and spleen derived macrophages of LD-infected BALB/c mice. A two-fold increase in HIF-1α mRNA was detected in LD-infected macrophages suggesting involvement of a transcriptional mechanism that was confirmed by promoter activity. We further revealed that LD also induced HIF-1α expression by depleting host cellular iron pool to affect prolyl hydroxylase activity resulting in to stabilization of HIF-1α. To determine the role of HIF-1 on intracellular LD, cells were transfected with HIF-1α siRNA to attenuate its expression and then infected with LD. Although, initial infection rate of LD in HIF-1α attenuated cells was not affected but intracellular growth of LD was significantly inhibited; while, over-expression of stabilized form of HIF-1α promoted intracellular growth of LD in host macrophage. Our results strongly suggest that LD activates HIF-1 by dual mechanism for its survival advantage within macrophage.
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