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In the present paper we focused on the potential role of human lactoferrin for the intracellular replication rate of T. gondii BK tachyzoites following our earlier observation that Toxoplasma gondii was able to bind human lactoferrin but not serum transferrin. The study was performed in vitro on human CaCo-2 epithelial cells and mouse L929 fibroblasts. We found that the multiplication of the parasite was inhibited by lactoferrin in both cell lines used. However, the direct cytotoxic effect on the parasite and the host cells was not observed. The intracellular growth of T. gondii was not affected when tachyzoites or host cells were only pre-coated with human lactoferrin. The results suggest that lactoferrin does not influence parasites penetration into host cells but could trigger unknown antiparasitic mechanisms in the infected cells.
Ethambutol (EMB) is a first line drug in tuberculosis treatment inhibiting the biosynthesis of arabinogalactan, which is a component of the mycobacterial cell wall. The growth of Mycobacterium vaccae cells in the presence of EMB increases cell wall permeability, which was monitored by β-sitosterol biotransformation. GC/MS and GLC/MS (gas chromatography/mass spectrometry) analysis revealed dramatic changes in the content of covalently bound mycolic acids and in molar ratio galactose (Gal) to arabinose (Ara) in the cell envelopes of EMB-treated cells. The detected variations in the compositions of fatty acids indicate that both the cell wall skeleton and outer layer (free lipids) are decomposed due to EMB treatment.
Ethambutol (EMB), the first line drug in the treatment of tuberculosis, is an inhibitor of the biosynthesis of the cell wall compound - arabinogalactan. It was found that EMB at sub-inhibitory concentration increases the permeability of the M. vaccae cell wall, which was monitored by cell sensitization to erythromycin and rifampicin. The high permeability of the cell wall to hydrophobic compounds allows enhanced intracellular bioconversion of (β -sitosterol to 4-androsten-3,17-dione (AD) and l,4-androstadien-3,17-dione (ADD).
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