linoleic-acid and Schistosomiasis-mansoni

It has been observed that fluorescent membrane-impermeant molecules can enter the cercariae as they penetrate mouse skin. The hypothesis to be tested was that such molecules, which included Lucifer Yellow and a variety of fluorescent dextrans, entered the parasite through the nephridiopore and excretory tubules as well as through the surface membrane. FITC-labelled poly-L-lysine (molecular weight 10 kDa), added at 4 degrees C during syringe transformation, was found to enter the nephridiopore and labelled the excretory bladder and sometimes the excretory tubules. This finding indicates that macromolecules (10 kDa) can enter the nephridiopore. It was found that linoleic acid (a normal constituent of skin) greatly stimulated uptake of Lucifer Yellow and dextrans into the excretory/subtegumental region of 2-h-old schistosomula. This correlated with an increased uptake of membrane-impermeant propidium iodide at 37 degrees C. Since increased uptake of propidium iodide occurs when membranes become permeable, the surface membrane could also be a pathway of transport of the membrane-impermeant molecules into the schistosomulum.

Topics: Animals; Biological Transport; Dextrans; Fluorescent Dyes; Host-Parasite Interactions; Humans; Isoquinolines; Larva; Linoleic Acid; Macromolecular Substances; Schistosoma mansoni; Schistosomiasis mansoni; Skin

The fatty acid status of mice six weeks after infection with Schistosoma mansoni was investigated and compared with the status of uninfected mice. Fatty acids of several plasma and erythrocyte lipid fractions were determined by capillary gas-chromatography. Major fatty acids including linoleic acid, arachidonic acid and dihomo-gamma-linolenic acid, were significantly reduced in the plasma phospholipids of infected mice. Arachidonic acid was also reduced in plasma cholesterolesters. The degree of the plasma arachidonic acid reduction in infected animals correlated neither with the worm load nor with the liver weight. The plasma fatty acid changes were not reflected in the lipids of the red blood cells. Since the observed changes in the plasma fatty acid composition occurred early after infection, they are unlikely to be a consequence of portal hypertension. It is speculated that an activation of the eicosanoid metabolism may contribute to these changes.

Topics: Animals; Arachidonic Acid; Cholesterol Esters; Eicosanoids; Erythrocytes; Fatty Acids; Female; Linoleic Acid; Linoleic Acids; Liver; Mice; Organ Size; Plasma; Schistosoma mansoni; Schistosomiasis mansoni