Leishmania–Host-cell Interaction: Complexities and Alternative Views

Rittig, Michael; Bogdan, Christian

doi:10.1016/s0169-4758(00)01692-6

Cited by 194 publications

(142 citation statements)

References 56 publications

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“…Amastigotes Residing within J774A.1 Cells-Host cell entry by promastigote protozoa involves the formation of membranebound PVs, where they transform into the immotile amastigote forms (25). The success of these organisms in surviving within the PVs determines pathogenesis of a disease.…”

Section: Potassium Antimony Tartrate Is Cytotoxic To L Donovanimentioning

confidence: 99%

Antimonial-induced Increase in Intracellular Ca2+ through Non-selective Cation Channels in the Host and the Parasite Is Responsible for Apoptosis of Intracellular Leishmania donovani Amastigotes

Sudhandiran

Shaha

2003

Journal of Biological Chemistry

158

126

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The capability of the obligate intracellular parasites like Leishmania donovani to survive within the host cell parasitophorous vacuoles as nonmotile amastigotes determines disease pathogenesis, but the mechanism of elimination of the parasites from these vacuoles are not well understood. By using the anti-leishmanial drug potassium antimony tartrate, we demonstrate that, upon drug exposure, intracellular L. donovani amastigotes undergo apoptotic death characterized by nuclear DNA fragmentation and externalization of phosphatidylserine. Changes upstream of DNA fragmentation included generation of reactive oxygen species like superoxide, nitric oxide, and hydrogen peroxide that were primarily concentrated in the parasitophorous vacuoles. In the presence of antioxidants like N-acetylcysteine or Mn(III) tetrakis(4-benzoic acid)porphyrin chloride, an inhibitor of inducible nitric-oxide synthase, a diminution of reactive oxygen species generation and improvement of amastigote survival were observed, suggesting a close link between drug-induced oxidative stress and amastigote death. Changes downstream to reactive oxygen species increase involved elevation of intracellular Ca 2؉ concentrations in both the parasite and the host that was preventable by antioxidants. Flufenamic acid, a non-selective cation channel blocker, decreased the elevation of Ca 2؉ in both the cell types and reduced amastigote death, thus establishing a central role of Ca 2؉ in intracellular parasite clearance. This influx of Ca 2؉ was preceded by a fall in the amastigote mitochondrial membrane potential. Therefore, this study projects the importance of flufenamic acid-sensitive non-selective cation channels as important modulators of antimonial efficacy and lends credence to the suggestion that, within the host cell, apoptosis is the preferred mode of death for the parasites.

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Section: Potassium Antimony Tartrate Is Cytotoxic To L Donovanimentioning

confidence: 99%

Antimonial-induced Increase in Intracellular Ca2+ through Non-selective Cation Channels in the Host and the Parasite Is Responsible for Apoptosis of Intracellular Leishmania donovani Amastigotes

Sudhandiran

Shaha

2003

Journal of Biological Chemistry

158

126

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“…Such organisms have adopted different strategies to survive within M. For example, Listeria monocytogenes and Trypanosoma cruzi escape the phagolysosome and reside within the cytoplasm (3,4). In contrast, Leishmania major and Mycobacterium tuberculosis, through distinct molecular strategies, are able to survive within modified phagosomes (5)(6)(7). In addition, L. major promastigotes have been shown to selectively suppress M IL-12 production, although the molecular details of this phenomenon remain enigmatic (8 -10).…”

Section: Acrophages (M)mentioning

confidence: 99%

Toxoplasma gondiiTachyzoites Inhibit Proinflammatory Cytokine Induction in Infected Macrophages by Preventing Nuclear Translocation of the Transcription Factor NF-κB

Butcher

Kim

Johnson

et al. 2001

The Journal of Immunology

191

185

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Control of microbial infection requires regulated induction of NF-κB-dependent proinflammatory cytokines such as IL-12 and TNF-α. Activation of this important transcription factor is driven by phosphorylation-dependent degradation of the inhibitory IκB molecule, an event which enables NF-κB translocation from the cytoplasm to the nucleus. In this study, we show that intracellular infection of macrophages with the protozoan parasite Toxoplasma gondii induces rapid IκB phosphorylation and degradation. Nevertheless, NF-κB failed to translocate to the nucleus, enabling the parasite to invade cells without triggering proinflammatory cytokine induction. Infected cells subsequently subjected to LPS triggering were severely crippled in IL-12 and TNF-α production, a result of tachyzoite-induced blockade of NF-κB nuclear translocation. Our results are the first to demonstrate the ability of an intracellular protozoan to actively interfere with the NF-κB activation pathway in macrophages, an activity that may enable parasite survival within the host.

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“…11 In the literature, it has been shown that parasites infect not only professional phagocytotic cells such as macrophages but also amnion epithelial cells, fibroblasts, kidney cells, and dendritic cells in mammalian hosts. 11,12 Furthermore, it is documented that parasites enter these cells by binding different cell surface receptors. Although there are many studies that investigate cellular and molecular characteristics of mesenchymal stem cells, the information about the phagocytic properties of these cells is scarce.…”

Section: Discussionmentioning

confidence: 99%

“…12 Stem cells have the ability of self-renewal and differentiate into a variety of other cell types in a given tissue. 13 Bone marrow-derived mesenchymal stem cells have become a major stem cell source in both research and therapeutic studies for years.…”

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confidence: 99%

Adipose Tissue-Derived Mesenchymal Stem Cells as a New Host Cell in Latent Leishmaniasis

Allahverdiyev¹,

Bağırova²,

Elcicek³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Some protozoan infections such as Toxoplasma, Cryptosporidium, and Plasmodium can be transmitted through stem cell transplantations. To our knowledge, so far, there is no study about transmission of Leishmania parasites in stem cell transplantation and interactions between parasites and stem cells in vitro. Therefore, the aim of this study was to investigate the interaction between different species of Leishmania parasites and adipose tissue-derived mesenchymal stem cells (ADMSCs). ADMSCs have been isolated, cultured, characterized, and infected with different species of Leishmania parasites (L. donovani, L. major, L. tropica, and L. infantum). Infectivity was examined by Giemsa staining, microculture, and polymerase chain reaction methods. As a result, infectivity of ADMSCs by Leishmania parasites has been determined for the first time in this study. According to our findings, it is very important that donors are screened for Leishmania parasites before stem cell transplantations in regions where leishmaniasis is endemic.

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Leishmania–Host-cell Interaction: Complexities and Alternative Views

Cited by 194 publications

References 56 publications

Antimonial-induced Increase in Intracellular Ca2+ through Non-selective Cation Channels in the Host and the Parasite Is Responsible for Apoptosis of Intracellular Leishmania donovani Amastigotes

Antimonial-induced Increase in Intracellular Ca2+ through Non-selective Cation Channels in the Host and the Parasite Is Responsible for Apoptosis of Intracellular Leishmania donovani Amastigotes

Toxoplasma gondiiTachyzoites Inhibit Proinflammatory Cytokine Induction in Infected Macrophages by Preventing Nuclear Translocation of the Transcription Factor NF-κB

Adipose Tissue-Derived Mesenchymal Stem Cells as a New Host Cell in Latent Leishmaniasis

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