Your browser doesn't support javascript.
loading
Montrer: 20 | 50 | 100
Résultats 1 - 2 de 2
Filtre
Ajouter des filtres








Gamme d'année
1.
Indian J Exp Biol ; 2014 Jan; 52(1): 17-29
Article Dans Anglais | IMSEAR | ID: sea-150328

Résumé

In experimental visceral leishmaniasis the causative obligate protozoan parasite, L. donovani invades and multiplies inside of macrophages, one of the sentries of the mammalian immune system. The initial host-parasite interaction between the Leishmania promastigote and the macrophage takes place at the plasma membrane interface. To trace any possible interaction between Toll-like receptor 2 (TLR2) and CC chemokine receptor 5 (CCR5) during early Leishmania-macrophage interactions, it was observed that the expression of both TLR2 and CCR5 were significantly increased, along with their recruitment to the lipid raft. TLR2 silencing attenuates CCR5 expression and restricts L. donovani infection, indicating a regulatory role of TLR2 and CCR5 during infection. Silencing of CCR5 and TLR2 markedly reduced the number of intracellular parasites in macrophages by host protective cytokine responses, while raft disruption using β-MCD affected TLR2/CCR5 cross-talk and resulted in a significant reduction in parasite invasion. In vivo RNA interference of TLR2 and CCR5 using shRNA plasmids rendered protection in Leishmania donovani-infected mice. Thus, this study for the first time demonstrates the importance of TLR2/CCR5 crosstalk as a significant determinant of Leishmania donovani entry in host macrophages.


Sujets)
Animaux , Interactions hôte-parasite , Humains , Infections/métabolisme , Infections/parasitologie , Leishmania donovani/métabolisme , Leishmania donovani/pathogénicité , Leishmaniose viscérale/métabolisme , Leishmaniose viscérale/parasitologie , Macrophages/métabolisme , Microdomaines membranaires , Souris , Récepteurs CCR5/métabolisme , Récepteur de type Toll-2/métabolisme
2.
Indian J Biochem Biophys ; 2007 Oct; 44(5): 366-72
Article Dans Anglais | IMSEAR | ID: sea-28766

Résumé

Arabinosylated lipoarabinomannan (Ara-LAM), a surface glycolipid antigen isolated from avirulent Mycobacterium smegmatis is involved in modulation of host cell signaling. In this study, we investigated Ara-LAM-mediated modulation of impaired immune responses during visceral leishmaniasis caused by protozoan parasite Leishmania donovani. Ara-LAM treatment at dose of 3 microg/ml in L. donovani infected murine peritoneal macrophages as well as J774A.1 macrophage cell line exhibited a distinct up-regulation of pro-inflammatory cytokines like TNF-alpha and IL-12 both at the protein and transcriptional level. In addition, generation of nitric oxide and iNOS expression were also observed. The present study showed that Ara-LAM was significantly effective in elimination of L. donovani parasites from both peritoneal as well as J774A.1 macrophages. Thus, it could be utilized as an immunomodulatory agent in prevention of leishmanial pathogenesis.


Sujets)
Animaux , Cellules cultivées , Relation dose-effet des médicaments , Immunité innée/effets des médicaments et des substances chimiques , Facteurs immunologiques/administration et posologie , Leishmania donovani/immunologie , Lipopolysaccharides/administration et posologie , Macrophages/effets des médicaments et des substances chimiques , Souris , Souris de lignée BALB C
SÉLECTION CITATIONS
Détails de la recherche