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leishmaniasis/hypoxia
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Expression on hypoxia-inducible factor-1α in human tegumentary leishmaniosis caused by Leishmania braziliensis
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Several immune markers have been studied in controlling American tegumentary leishmaniosis based on mouse models. However, there is a lack of studies regarding human tegumentary leishmaniosis caused by Leishmania braziliensis. In this study, hypoxia-inducible factor-1α was found to be an important
Hypoxia modulates expression of the 70-kD heat shock protein and reduces Leishmania infection in macrophages.
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Hypoxia, a microenvironmental factor present in diseased tissues, has been recognized as a specific metabolic stimulus or a signal of cellular response. Experimental hypoxia has been reported to induce adaptation in macrophages such as differential migration, elevation of proinflammatory cytokines
Infection by Leishmania amazonensis in mice: a potential model for chronic hypoxia.
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Hypoxia is a common feature of injured and infected tissues. Hypoxia inducible factors 1α and 2α (HIF-1α, HIF-2α) are heterodimeric transcription factors mediating the cellular responses to hypoxia and also the vascular endothelial growth factor (VEGF). VEGF is a cytokine which can be induced by
The influence of low oxygen on macrophage response to Leishmania infection.
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Hypoxia (low oxygen tension) is a common feature of inflamed and infected tissues. The influence of hypoxia on macrophage responses to micro-organisms has only recently been studied. This study demonstrates that hypoxia induced macrophages to control Leishmania amazonensis, an intracellular parasite
Functional alterations in macrophages after hypoxia selection.
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Regions of low oxygen tension are common features of inflamed and infected tissues and provide physiologic selective pressure for the expansion of cells with enhanced hypoxia tolerance. The aim of this study was to investigate whether macrophages resistant to death induced by hypoxia were
Immunohistochemical evidence of stress and inflammatory markers in mouse models of cutaneous leishmaniosis.
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Leishmanioses are chronic parasitic diseases and host responses are associated with pro- or anti-inflammatory cytokines involved, respectively, in the control or exacerbation of infection. The relevance of other inflammatory mediators and stress markers has not been widely studied and there is a
Evaluation of hypoxia inducible factor targeting pharmacological drugs as antileishmanial agents.
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OBJECTIVE
To evaluate whether hypoxia inducible factor (HIF-1α) targeting pharmacological drugs, echinomycin, resveratrol and CdCl2 which inhibit HIF-1α stimulation, and mimosine, which enhances the stability of HIF-1α present antileishmanial properties.
METHODS
The leishmanicidal effect of drugs
Intracellular pathogen Leishmania donovani activates hypoxia inducible factor-1 by dual mechanism for survival advantage within macrophage.
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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
Leishmania donovani Activates Hypoxia Inducible Factor-1α and miR-210 for Survival in Macrophages by Downregulation of NF-κB Mediated Pro-inflammatory Immune Response.
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Micro RNAs (miRNAs) have emerged as a critical regulator of several biological processes in both animals and plants. They have also been associated with regulation of immune responses in many human diseases during recent years. Visceral leishmaniasis (VL) is the most severe form of leishmaniasis,
HIF-1α is a key regulator in potentiating suppressor activity and limiting the microbicidal capacity of MDSC-like cells during visceral leishmaniasis.
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Leishmania donovani is known to induce myelopoiesis and to dramatically increase extramedullary myelopoiesis. This results in splenomegaly, which is then accompanied by disruption of the splenic microarchitecture, a chronic inflammatory environment, and immunosuppression. Chronically inflamed
HIF-1α hampers dendritic cell function and Th1 generation during chronic visceral leishmaniasis.
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Inflammation, although responsible for controlling infection, is often associated with the pathogenesis of chronic diseases. Leishmania donovani, the causative agent of visceral leishmaniasis, induces a strong inflammatory response that leads to splenomegaly and ultimately immune suppression.
Resolution of Cutaneous Leishmaniasis and Persistence of Leishmania major in the Absence of Arginase 1.
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Arginase (Arg) 1 is expressed by hematopoietic (e.g., macrophages) and nonhematopoietic cells (e.g., endothelial cells) and converts l-arginine into ornithine and urea. The enzyme is implicated in tissue repair but also antagonizes the production of NO by type 2 NO synthase in myeloid cells and
Mucocutaneous leishmaniasis in guinea-pigs inoculated intravenously with Leishmania enriettii. Preliminary report.
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Seven guinea-pigs were inoculated intravenously with a rich suspension of Leishmania enriettii. During the sixth to the seventh week from inoculation, all of them developed lesions within the anterior nasal mucosa and in the vulva or scrotum. In one animal nodules occurred in the forepaws during the
Unveiling the Role of the Integrated Endoplasmic Reticulum Stress Response in Leishmania Infection - Future Perspectives.
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The integrated endoplasmic reticulum stress response (IERSR) is an evolutionarily conserved adaptive mechanism that ensures endoplasmic reticulum (ER) homeostasis and cellular survival in the presence of stress including nutrient deprivation, hypoxia, and imbalance of Ca(+) homeostasis, toxins, and
Myeloid Cell-Derived HIF-1α Promotes Control of Leishmania major.
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Hypoxia-inducible factor-1α (HIF-1α), which accumulates in mammalian host organisms during infection, supports the defense against microbial pathogens. However, whether and to what extent HIF-1α expressed by myeloid cells contributes to the innate immune response against Leishmania major parasites
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