Trypanosoma cruzi: Participation of cholesterol and placental alkaline phosphatase in the host cell invasion

• Published in: Experimental parasitology Vol. 122; no. 1; pp. 70 - 73
• Main Authors: Priotto, S., Sartori, M.J., Repossi, G., Valentich, M.A.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.05.2009; Elsevier
• Subjects: Alkaline Phosphatase - metabolism; Animals; Anticholesteremic Agents - pharmacology; beta-Cyclodextrins - pharmacology; Biological and medical sciences; Cell Line; Cholesterol; Cholesterol - metabolism; Fundamental and applied biological sciences. Psychology; Gamma glutamyltranspeptidase; gamma-Glutamyltransferase - metabolism; Humans; Life cycle. Host-agent relationship. Pathogenesis; Lovastatin - pharmacology; Membrane Microdomains - physiology; Mice; Placental alkaline phosphatase; Protozoa; Trypanosoma cruzi; Trypanosoma cruzi - enzymology; Trypanosoma cruzi - physiology; Trypanosoma cruzi invasion; Placental alkaline phosphatase; Gamma glutamyltranspeptidase; Cholesterol; Trypanosoma cruzi invasion; Kinetoplastida; Protozoa; Alkaline phosphatase; Enzyme; Phosphoric monoester hydrolases; Parasite; Esterases; Host; Invasion; Trypanosoma cruzi; Hydrolases
• ISSN: 0014-4894; 1090-2449
• DOI: 10.1016/j.exppara.2009.01.004

One of the most important parasitic endemic diseases in Latin America is Chagas disease, with almost 20 million people being infected and 60 million others at risk of infection. In the cell infection by Trypanosoma cruzi, the first step is contact with the host cell by receptors and ligands on the membrane. It is known that lipids play an important role in the interaction process between pathogens and host cells with lipid rafts being highly specialized regions of the plasma membrane that are enriched in cholesterol and sphingolipids. We explored whether the treatment with methyl-beta-cyclodextrin alone or by adding Mevinolin, an inhibitor of cholesterol synthesis could deplete membrane cholesterol of the HEp2 cell and if this treatment could affect the trypomastigote infection into the host cell. These treatments led to a leakage of cholesterol, and concomitantly, PLAP enzyme and unidentified proteins resulting in a decrease of the invasion process. However, the GGTP enzyme was not liberated from the host cell membranes.