RETRACTED: Leishmania donovani Isolates with Antimony-Resistant but Not -Sensitive Phenotype Inhibit Sodium Antimony Gluconate-Induced Dendritic Cell Activation
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Dossier post-publication
- Nature
- Retraction
- Motif
- Concerns/Issues about Data;Duplication of Data;Euphemisms for Duplication;Investigation by Journal/Publisher;Investigation by Third Party;Manipulation of Data;Unreliable Results and/or Conclusions;
- Date
- 1/21/2026 0:00
- Signalé par OpenAlex ?
- Oui
Source : Retraction Watch, jointe par DOI. OpenAlex consigne la rétractation dans is_retracted, un booléen sur un espace d'états à au moins quatre valeurs ; il ne peut donc exprimer ni une expression de préoccupation, ni une correction, ni un rétablissement, et les rapporte comme false, ce qui se lit comme « rien à signaler ».
Résumé
The inability of sodium antimony gluconate (SAG)-unresponsive kala-azar patients to clear Leishmania donovani (LD) infection despite SAG therapy is partly due to an ill-defined immune-dysfunction. Since dendritic cells (DCs) typically initiate anti-leishmanial immunity, a role for DCs in aberrant LD clearance was investigated. Accordingly, regulation of SAG-induced activation of murine DCs following infection with LD isolates exhibiting two distinct phenotypes such as antimony-resistant (Sb(R)LD) and antimony-sensitive (Sb(S)LD) was compared in vitro. Unlike Sb(S)LD, infection of DCs with Sb(R)LD induced more IL-10 production and inhibited SAG-induced secretion of proinflammatory cytokines, up-regulation of co-stimulatory molecules and leishmanicidal effects. Sb(R)LD inhibited these effects of SAG by blocking activation of PI3K/AKT and NF-kappaB pathways. In contrast, Sb(S)LD failed to block activation of SAG (20 microg/ml)-induced PI3K/AKT pathway; which continued to stimulate NF-kappaB signaling, induce leishmanicidal effects and promote DC activation. Notably, prolonged incubation of DCs with Sb(S)LD also inhibited SAG (20 microg/ml)-induced activation of PI3K/AKT and NF-kappaB pathways and leishmanicidal effects, which was restored by increasing the dose of SAG to 40 microg/ml. In contrast, Sb(R)LD inhibited these SAG-induced events regardless of duration of DC exposure to Sb(R)LD or dose of SAG. Interestingly, the inhibitory effects of isogenic Sb(S)LD expressing ATP-binding cassette (ABC) transporter MRPA on SAG-induced leishmanicidal effects mimicked that of Sb(R)LD to some extent, although antimony resistance in clinical LD isolates is known to be multifactorial. Furthermore, NF-kappaB was found to transcriptionally regulate expression of murine gammaglutamylcysteine synthetase heavy-chain (mgammaGCS(hc)) gene, presumably an important regulator of antimony resistance. Importantly, Sb(R)LD but not Sb(S)LD blocked SAG-induced mgammaGCS expression in DCs by preventing NF-kappaB binding to the mgammaGCS(hc) promoter. Our findings demonstrate that Sb(R)LD but not Sb(S)LD prevents SAG-induced DC activation by suppressing a PI3K-dependent NF-kappaB pathway and provide the evidence for differential host-pathogen interaction mediated by Sb(R)LD and Sb(S)LD.
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La notice
- Revue
- PLoS Pathogens
- Thématique
- Research on Leishmaniasis Studies
- Domaine
- Medicine
- Établissements canadiens
- —
- Organismes subventionnaires
- CSIR - Institute of Microbial TechnologyUniversität WienBanaras Hindu UniversityCentral Drug Research InstituteUniversité LavalCouncil of Scientific and Industrial Research, IndiaMedizinische Universität Wien
- Mots-clés
- Leishmania donovaniPI3K/AKT/mTOR pathwayProtein kinase BImmune systemProinflammatory cytokineLeishmaniaBiologyChemistryPharmacologySignal transductionCell biologyImmunologyLeishmaniasisVisceral leishmaniasisInflammation
- Résumé présent dans OpenAlex
- oui