RESUMEN
One of the mechanisms by which adjuvants are believed to promote T-cell activation and prevent induction of oral tolerance is by up-regulating the expression of co-stimulatory molecules on antigen presenting cells. Mice treated orally with palmitoyl-ovalbumin conjugates become immunized, while those treated with native ovalbumin (Ova) become tolerant. Cells from the peritoneal cavity of B6D2F1 mice were cultured in the presence of 0.01, or 0.1 mg/100ml of either Ova, or palmitoyl-Ova and tested for the presence of cell markers. PE-conjugated anti-mouse CD80, CD86, and CD11b antibodies as well as biotin-PE were used to stain the antigen-activated peritoneal cells. A significant increase in the expression of CD86 and CD80 was observed following in vitro stimulation with palmitoyl-Ova; additionally, both Ova and palmitoyl-Ova induced the basal expression of CD11b. These findings could be related with the strong T-cell proliferative response induced by palmitoyl-Ova.
RESUMEN
The aim of this work was to evaluate the effects of ethanol on the adsorption and tissue distribution of orally administered antigens in mice. Results showed that ethanol reduced the level of anti-ovalbumin IgA antibodies in intestinal fluid for the mice treated orally with a palmitoyl-ovalbumin conjugate. Ethanol was administered intragastrically to mice at 5 g/kg body weight for 14 days (chronic treatment), or 10 g/kg body weight every 7th day up to 14 days (acute treatment). Thereafter, 99m technetium-labeled antigens were administered and lymphoid tissues were collected. Ethanol interfered with the transport of ovalbumin to the liver. Moreover, the transport of palmitoyl-ovalbumin to mesenteric lymph nodes was reduced 6 h after the antigen administration. In conclusion, there was a relationship between the suppression of ethanol-mediated specific local IgA responses and the decreased transport of palmitoyl-ovalbumin to mesenteric lymph nodes.