Transforming growth factor beta-1 (TGF-beta1) is a pleiotropic cytokine with both pro- and antiinflammatory properties, depending on its environment and concentration. The present study evaluated the effects of orally-delivered TGF-beta1 on mice parenterally-infected with various protozoan parasites. We report that while orally-administered TGF-beta1 seems to confer partial protection against murine chronic babesiosis and acute trypanosomosis, no beneficial clinical effects were observed against acute babesiosis, malaria or toxoplasmosis. Taken together, these preliminary data suggest that the systemic effects conferred by exogenous TGF-beta1 could be parasite species-specific. The variations in different parasitic infections could be due to (i) intrinsic differences between parasite species and/or strains in their ability to induce production of immunosuppressive molecules and/or (ii) differences in mechanisms governing host protection against different parasitic infections.

The major cause of infection in animal prion diseases is thought to be consumption of prion-contaminated stuff. There is evidence that the enteric nerve system (ENS) and gut-associated lymphoid tissues (GATL) are involved in the establishment of prion infection through alimentary tract. To elucidate the initial entry port for prion, we inoculated prion to alymphoplasia (aly) mice showing a deficiency in systemic lymph nodes and Peyer's patches. The aly/aly mice were susceptible to prion infection by intra-cranial inoculation and there were no differences in incubation periods between aly/aly mice and wild-type C57BL/6J mice. Incubation periods in aly/aly mice were about 20 days longer than those in C57BL/6J mice with the intra-peritoneal inoculation. The aly/aly mice were completely resistant to prion infection by per os administration, while C57BL/6J mice were sensitive as they entered the terminal stage of disease around 300 days post inoculation. PrPsup(sc) were detected in the intestine and spleen of C57BL/6J mice inoculated with prion intra-peritoneally or orally; however PrPsup(sc) was not detected in the spleen and intestine of aly/aly mice. Prion infectivity was detected in the intestines and spleens of prion-inoculated C57BL/6J mice, even after the early stages of ex-posure, while no infectivity was detected in these tissues of prion-inoculated aly/aly mice. No apparent differences were observed in the organization of the enteric nerve system between wild-type and aly/aly mice. These results indicate that GALT rather than ENS acts as the primary entry port for prion after oral exposure.