| Autor: |
Maldonado-Bernal, C., Kirschning, C. J., Rosenstein, Y., Rocha, L. M., Rios-Sarabia, N., Espinosa-Cantellano, M., Becker, I., Estrada, I., Salazar-González, R. M., López-Macías, C., Wagner, H., Sánchez, J., Isibasi, A. |
| Předmět: |
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| Zdroj: |
Parasite Immunology; Apr2005, Vol. 27 Issue 4, p127-137, 11p |
| Abstrakt: |
Entamoeba histolyticais a human pathogen that may invade the intestinal mucosa, causing amoebic colitis or hepatic abscesses when the trophozoites travel through the portal circulation to the liver. Lipopeptidophosphoglycan (LPPG) is a molecular pattern ofE. histolyticarecognized by the human immune system. Here we report that LPPG is exposed on the cell surface ofE. histolyticatrophozoites, and is recognized by the host through toll-like receptor (TLR) 2 and TLR4. Correspondingly, human embryonic kidney (HEK)-293 cells were rendered LPPG responsive through overexpression of TLR2 or TLR4/MD2. Moreover, co-expression of CD14 enhanced LPPG signal transmission through TLR2 and TLR4. The interaction of LPPG with TLR2 and TLR4 resulted in activation of NF-κB and release of interleukin (IL)-10, IL-12p40, tumour necrosis factor (TNF)-α, and IL-8 from human monocytes. Consistent with these findings, responsiveness of mouse macrophages lacking TLR2 expression (TLR2 –/– ) or functional TLR4 (TLR4 d/d ) toE. histolyticaLPPG challenge was impaired while double deficient macrophages were unresponsive. In contrast to wild-type control and TLR2 –/– animals succumbing to lethal shock syndrome, TLR4 d/d mice were resistant to systemic LPPG challenge-induced pathology. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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