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3. Correction for Abhishek et al., “Phosphorylation of Translation Initiation Factor 2-Alpha in Leishmania donovani under Stress Is Necessary for Parasite Survival”

Author

Abhishek, Kumar, primary, Sardar, Abul Hasan, additional, Das, Sushmita, additional, Kumar, Ashish, additional, Ghosh, Ayan Kumar, additional, Singh, Ruby, additional, Saini, Savita, additional, Mandal, Abhishek, additional, Verma, Sudha, additional, Kumar, Ajay, additional, Purkait, Bidyut, additional, Dikhit, Manas Ranjan, additional, and Das, Pradeep, additional

Published
2022
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7. Corrigendum: l-Arginine Uptake by Cationic Amino Acid Transporter Promotes Intra-Macrophage Survival of Leishmania donovani by Enhancing Arginase-Mediated Polyamine Synthesis

Author

Mandal, Abhishek, primary, Das, Sushmita, additional, Kumar, Ajay, additional, Roy, Saptarshi, additional, Verma, Sudha, additional, Ghosh, Ayan Kumar, additional, Singh, Ruby, additional, Abhishek, Kumar, additional, Saini, Savita, additional, Sardar, Abul Hasan, additional, Purkait, Bidyut, additional, Kumar, Ashish, additional, Mandal, Chitra, additional, and Das, Pradeep, additional

Published
2020
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9. l-Arginine Uptake by Cationic Amino Acid Transporter Promotes Intra-Macrophage Survival of Leishmania donovani by Enhancing Arginase-Mediated Polyamine Synthesis

Author

Mandal, Abhishek, primary, Das, Sushmita, additional, Kumar, Ajay, additional, Roy, Saptarshi, additional, Verma, Sudha, additional, Ghosh, Ayan Kumar, additional, Singh, Ruby, additional, Abhishek, Kumar, additional, Saini, Savita, additional, Sardar, Abul Hasan, additional, Purkait, Bidyut, additional, Kumar, Ashish, additional, Mandal, Chitra, additional, and Das, Pradeep, additional

Published
2017
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10. Phosphorylation of Translation Initiation Factor 2-Alpha in Leishmania donovani under Stress Is Necessary for Parasite Survival

Author

Abhishek, Kumar, primary, Sardar, Abul Hasan, additional, Das, Sushmita, additional, Kumar, Ashish, additional, Ghosh, Ayan Kumar, additional, Singh, Ruby, additional, Saini, Savita, additional, Mandal, Abhishek, additional, Verma, Sudha, additional, Kumar, Ajay, additional, Purkait, Bidyut, additional, Dikhit, Manas Ranjan, additional, and Das, Pradeep, additional

Published
2017
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12. Deprivation of L-Arginine Induces Oxidative Stress Mediated Apoptosis in Leishmania donovani Promastigotes: Contribution of the Polyamine Pathway

Author

Mandal, Abhishek, primary, Das, Sushmita, additional, Roy, Saptarshi, additional, Ghosh, Ayan Kumar, additional, Sardar, Abul Hasan, additional, Verma, Sudha, additional, Saini, Savita, additional, Singh, Ruby, additional, Abhishek, Kumar, additional, Kumar, Ajay, additional, Mandal, Chitra, additional, and Das, Pradeep, additional

Published
2016
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16. Unmethylated CpG motifs in the L. donovaniDNA regulate TLR9‐dependent delay of programmed cell death in macrophages

Author

Das, Sushmita, Ghosh, Ayan Kumar, Singh, Shikha, Saha, Bhaskar, Ganguly, Ashish, and Das, Pradeep

Abstract

Species‐specific unmethylated CpG‐motifs in L. donovaniDNA in modulating macrophage apoptosis through TLR9 and activation of the PI3K/Akt pathway. Regulation of macrophage PCD plays an important role in pathogenesis of leishmaniasis. However, the precise involvement of any parasite molecule in this process remains uncertain. In the current study, in silico wide analysis demonstrated that genes in the Leishmania donovanigenome are highly enriched for CpG motifs, with sequence frequency of 8.7%. Here, we show that unmethylated species‐specific CpG motifs in LdDNA significantly (P= 0.01) delay macrophage PCD by endosomal interaction with TLR9 via the adaptor protein MyD88. Importantly, LdDNA triggered high levels of luciferase activity (P= 0.001) under NF‐κB‐dependent transcription in HEK‐TLR9 cells. Furthermore, the activation of caspases in macrophages was inhibited (P= 0.001) in the presence of LdDNA. Notably, the delay of PCD was mediated by modulation of the antiapoptotic proteins, Mcl‐1 and Bfl‐1, and impairment of loss of Δψm in macrophages through the neutralization of oxidative and nitrosative stress. The inhibition of caspase activation and up‐regulation of Mcl‐1 by LdDNA were TLR9 dependent. Analysis of the targets of LdDNA identified an early activation of the TLR9‐dependent PI3K/Akt and SFK pathways, which were required for the observation of the antiapoptotic effects in macrophages. Moreover, we demonstrate that LdDNA modulates the TLR9–IκB‐αpathway by promoting the tyrosine phosphorylation of TLR9 and the TLR9‐mediated recruitment of Syk kinase. The results have identified a novel, TLR9‐dependent antiapoptotic function of LdDNA, which will provide new opportunities for discovering and evaluating molecular targets for drug and vaccine designing against VL.

Published
2015
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17. Phosphorylation of Translation Initiation Factor 2-Alpha in Leishmania donovani under Stress Is Necessary for Parasite Survival.

Author

Abhishek K, Sardar AH, Das S, Kumar A, Ghosh AK, Singh R, Saini S, Mandal A, Verma S, Kumar A, Purkait B, Dikhit MR, and Das P

Subjects
Adenine analogs & derivatives, Adenine pharmacology, Animals, Gene Expression Regulation, Hot Temperature, Hydrogen Peroxide pharmacology, Hydrogen-Ion Concentration, Indoles pharmacology, Leishmania donovani pathogenicity, Leishmaniasis metabolism, Life Cycle Stages, Mice, Oxidative Stress, Phosphorylation, Protozoan Proteins metabolism, Eukaryotic Initiation Factor-2 metabolism, Leishmania donovani physiology, Leishmaniasis parasitology, Stress, Physiological
Abstract

The transformation of Leishmania donovani from a promastigote to an amastigote during mammalian host infection displays the immense adaptability of the parasite to survival under stress. Induction of translation initiation factor 2-alpha (eIF2α) phosphorylation by stress-specific eIF2α kinases is the basic stress-perceiving signal in eukaryotes to counter stress. Here, we demonstrate that elevated temperature and acidic pH induce the phosphorylation of Leishmania donovani eIF2α (LdeIF2α). In vitro inhibition experiments suggest that interference of LdeIF2α phosphorylation under conditions of elevated temperature and acidic pH debilitates parasite differentiation and reduces parasite viability (P < 0.05). Furthermore, inhibition of LdeIF2α phosphorylation significantly reduced the infection rate (P < 0.05), emphasizing its deciding role in successful invasion and infection establishment. Notably, our findings suggested the phosphorylation of LdeIF2α under H 2 O 2 -induced oxidative stress. Inhibition of H 2 O 2 -induced LdeIF2α phosphorylation hampered antioxidant balance by impaired redox homeostasis gene expression, resulting in increased reactive oxygen species accumulation (P < 0.05) and finally leading to decreased parasite viability (P < 0.05). Interestingly, exposure to sodium antimony glucamate and amphotericin B induces LdeIF2α phosphorylation, indicating its possible contribution to protection against antileishmanial drugs in common use. Overall, the results strongly suggest that stress-induced LdeIF2α phosphorylation is a necessary event for the parasite life cycle under stressed conditions for survival., (Copyright © 2016 American Society for Microbiology.)

Published
2016
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18. Unmethylated CpG motifs in the L. donovani DNA regulate TLR9-dependent delay of programmed cell death in macrophages.

Author

Das S, Ghosh AK, Singh S, Saha B, Ganguly A, and Das P

Subjects
Apoptosis drug effects, Caspases immunology, DNA, Protozoan pharmacology, Enzyme Activation immunology, Female, HEK293 Cells, Humans, Macrophages cytology, Male, Myeloid Cell Leukemia Sequence 1 Protein immunology, Myeloid Differentiation Factor 88 immunology, Phosphorylation immunology, Up-Regulation immunology, Apoptosis immunology, CpG Islands immunology, DNA Methylation, DNA, Protozoan immunology, Leishmania donovani immunology, Macrophages immunology, Toll-Like Receptor 9 immunology
Abstract

Regulation of macrophage PCD plays an important role in pathogenesis of leishmaniasis. However, the precise involvement of any parasite molecule in this process remains uncertain. In the current study, in silico wide analysis demonstrated that genes in the Leishmania donovani genome are highly enriched for CpG motifs, with sequence frequency of 8.7%. Here, we show that unmethylated species-specific CpG motifs in LdDNA significantly (P = 0.01) delay macrophage PCD by endosomal interaction with TLR9 via the adaptor protein MyD88. Importantly, LdDNA triggered high levels of luciferase activity (P = 0.001) under NF-κB-dependent transcription in HEK-TLR9 cells. Furthermore, the activation of caspases in macrophages was inhibited (P = 0.001) in the presence of LdDNA. Notably, the delay of PCD was mediated by modulation of the antiapoptotic proteins, Mcl-1 and Bfl-1, and impairment of loss of Δψm in macrophages through the neutralization of oxidative and nitrosative stress. The inhibition of caspase activation and up-regulation of Mcl-1 by LdDNA were TLR9 dependent. Analysis of the targets of LdDNA identified an early activation of the TLR9-dependent PI3K/Akt and SFK pathways, which were required for the observation of the antiapoptotic effects in macrophages. Moreover, we demonstrate that LdDNA modulates the TLR9-IκB-α pathway by promoting the tyrosine phosphorylation of TLR9 and the TLR9-mediated recruitment of Syk kinase. The results have identified a novel, TLR9-dependent antiapoptotic function of LdDNA, which will provide new opportunities for discovering and evaluating molecular targets for drug and vaccine designing against VL., (© Society for Leukocyte Biology.)

Published
2015
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