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  • Leishmania donovani infection down-regulates TLR2-stimulated IL-12p40 and activates IL-10 in cells of macrophage/monocytic lineage by modulating MAPK pathways through a contact-dependent mechanism.

Leishmania donovani infection down-regulates TLR2-stimulated IL-12p40 and activates IL-10 in cells of macrophage/monocytic lineage by modulating MAPK pathways through a contact-dependent mechanism.

Clinical and experimental immunology (2008-09-10)
Dinesh Chandra, Sita Naik
摘要

The failure of Leishmania, an intracellular pathogen, to stimulate a pro-inflammatory response following entry into macrophages has been well reported. This occurs in spite of the fact that ligands for the toll-like receptors (TLR) have been recently shown on the parasite surface and their role in disease protection well documented. The outcome of infection in leishmaniasis is determined by the Th1 versus Th2 nature of the effector response and the generation of IL-12 and IL-10 by the infected macrophages is important for this decision. We evaluated the effect of L. donovani infection of monocytes (cell line THP-1, and monocytes derived from human peripheral blood) on Pam3cys (TLR2 ligand) and lipopolysaccharide (TLR4 ligand) stimulated production of IL-12p40 and IL-10. L. donovani infection caused suppression of TLR2 and TLR4-stimulated IL-12p40, with an increase in IL-10 production. Parasites also modulated the TLR2-stimulated mitogen-activated protein kinase (MAPK) pathway by suppressing MAPK P(38) phosphorylation and activating extracellular regulated kinase (ERK)1/2 phosphorylation. These effects could be reversed either by using a MAPK P(38) activator, anisomycin, or ERK1/2 inhibitor, U0126. L. donovani caused modulation of TLR2-stimulated MAPK pathways in a contact-dependent mechanism. In addition parasite structural integrity but not viability was required for suppression of TLR2-stimulated IL-12p40 and activation of IL-10. These observations suggest that L. donovani has evolved survival strategies that subvert the pro-inflammatory response generated through TLRs.

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Sigma-Aldrich
RPMI-1640 培养基, With L-glutamine and sodium bicarbonate, liquid, sterile-filtered, suitable for cell culture
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RPMI-1640 培养基, With sodium bicarbonate, without L-glutamine, liquid, sterile-filtered, suitable for cell culture
SAFC
RPMI-1640 培养基, HEPES Modification, With 25 mM HEPES, without L-glutamine., liquid, sterile-filtered, suitable for cell culture
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RPMI-1640 培养基, With L-glutamine, without sodium bicarbonate, powder, suitable for cell culture
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RPMI-1640 培养基, Modified, with 20 mM HEPES and L-glutamine, without sodium bicarbonate, liquid, sterile-filtered, suitable for cell culture
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StableCell RPMI-1640, With stable glutamine and sodium bicarbonate, liquid, sterile-filtered, suitable for cell culture
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RPMI-1640 培养基, Modified, with sodium bicarbonate, without L-glutamine and phenol red, liquid, sterile-filtered, suitable for cell culture
Sigma-Aldrich
RPMI-1640 培养基, Modified, with L-glutamine, without phenol red and sodium bicarbonate, powder, suitable for cell culture
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RPMI-1640 培养基, With L-glutamine, without glucose and sodium bicarbonate, powder, suitable for cell culture
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RPMI-1640 培养基, HEPES Modification, with L-glutamine and 25mM HEPES, without sodium bicarbonate, powder, suitable for cell culture
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RPMI-1640 培养基, with 2.05 mM L-glutamine, with 25mM HEPES, liquid, sterile-filtered, suitable for cell culture
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RPMI-1640 培养基, 10 ×, Without L-glutamine, folic acid and sodium bicarbonate, liquid, sterile-filtered, suitable for cell culture
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RPMI-1640 培养基, Hybri-Max, Modified, with L-glutamine, 4500 mg/L glucose and 15mM HEPES, without sodium bicarbonate, powder, suitable for hybridoma
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Millipore
滤膜,硝化纤维, MF membrane, pore size 0.22 μm, diam. 293 mm

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