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The host-protective effect of arabinosylated lipoarabinomannan against Leishmania donovani infection is associated with restoration of IFN-γ responsiveness.
Chowdhury, Bidisha Paul; Bandyopadhyay, Syamdas; Das, Shibali; Majumder, Saikat; Jha, Mukesh Kumar; Majumdar, Suchandra Bhattacharyya; Saha, Bhaskar; Majumdar, Subrata.
Afiliación
  • Chowdhury BP; Division of Molecular Medicine, Bose Institute, Kolkata, India.
  • Bandyopadhyay S; Division of Molecular Medicine, Bose Institute, Kolkata, India.
  • Das S; Division of Molecular Medicine, Bose Institute, Kolkata, India.
  • Majumder S; Division of Molecular Medicine, Bose Institute, Kolkata, India.
  • Jha MK; Laboratory-V, National Centre for Cell Science (NCCS), Pune, Maharashtra, India.
  • Majumdar SB; Division of Molecular Medicine, Bose Institute, Kolkata, India.
  • Saha B; Laboratory-V, National Centre for Cell Science (NCCS), Pune, Maharashtra, India.
  • Majumdar S; Division of Molecular Medicine, Bose Institute, Kolkata, India.
PLoS One ; 10(2): e0117247, 2015.
Article en En | MEDLINE | ID: mdl-25658110
Visceral leishmaniasis (VL), which is endemic as a major infectious disease in the tropical and subtropical countries, is caused by a protozoan parasite Leishmania donovani. At present, restricted treatment options and lack of vaccines intensify the problem of controlling VL. Therefore, finding a novel immunoprophylactic or therapeutic principle is a pressing need. Here, we report that arabinosylated lipoarabinomannan (Ara-LAM), a TLR2-ligand isolated from Mycobacterium smegmatis, exhibits a strong immunomodulatory property that conferred protection against L. donovani infection. Although, Ara-LAM modulates TLR2 and MAPK signaling, it is not known whether Ara-LAM involves IFN-γ signaling for effective parasite clearance. Because, it is reported that IFN-γ signaling, a principle mediator of NO generation and macrophage and Tcell activation, is hampered during leishmanial pathogenesis. Ara-LAM increases IFN-γ receptor expression and potentiates IFN-γ receptor signaling through JAK-STAT pathway. Moreover, Ara-LAM reciprocally modulates IRF4 and IRF8 expression and reinstates anti-leishmanial Th1 response that eventuates in significantly reduced parasite load in spleen and liver of L. donovani-infected BALB/c mice. IFN-γRα silencing resulted in the suppression of these host-protective mechanisms affected by Ara-LAM. Thus, Ara-LAM-mediated restoration of IFN-γ responsiveness is a novel immuno-modulatory principle for protection against L. donovani susceptible host.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arabinosa / Leishmania donovani / Lipopolisacáridos / Interferón gamma / Receptor de Interferón alfa y beta / Interacciones Huésped-Patógeno / Leishmaniasis Visceral Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2015 Tipo del documento: Article País de afiliación: India Pais de publicación: Estados Unidos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Arabinosa / Leishmania donovani / Lipopolisacáridos / Interferón gamma / Receptor de Interferón alfa y beta / Interacciones Huésped-Patógeno / Leishmaniasis Visceral Tipo de estudio: Risk_factors_studies Límite: Animals Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2015 Tipo del documento: Article País de afiliación: India Pais de publicación: Estados Unidos