Biomedical subjects
Publications and source records attributed to J R Seed.
Daily administration of tryptophol to laboratory rodents resulted in significantly depressed antibody production of heterologous red blood cell challenge, did not alter cellular-mediated responses to oxazalone. These results suggest that trypanosome-produced tryptophol may account for the immunodepression observed during trypanosomiasis.
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Trypanosoma brucei gambiense infections in the field vole Microtus montanus increased susceptibility to Ehrlich's tumor growth. Whereas uninfected voles were totally resistant to intraperitoneal Ehrlich's ascites tumor cell challenge, over 78% of the animals infected with the trypanosomes developed tumors after challenge. Likewise, when Ehrlich's ascites cells were injected subcutaneously to induce solid tumor formation, only 7% of uninfected controls developed tumors, whereas over 82% of trypanosome-infected animals exhibited malignancies after Ehrlich's cell challenge. Finally, when solid tumors grown in albino CD-1 mice were implanted subcutaneously into uninfected voles, the tumor mass rapidly diminished in size and could not be found when animals were examined 2 weeks postimplant. However, in trypanosome-infected voles, implanted tumors exhibited pronounced expansion, and viable, solid tumors were recovered from over 70% of the challenged voles at 2 weeks postimplant. The implications of trypanosome-induced immunosuppression, especially toward susceptibility to neoplastic growth, are discussed.
The effects of Trypanosoma brucei gambiense infections upon immune responses were examined in an outbred laboratory colony of field voles. Microtus montanus. Antibody levels to challenge with heterologous erythrocytes and bovine serum albumin were significantly depressed in infected animals. Trypanosome infections impaired both primary and secondary humoral responses, although previously established specific antibody levels were not affected by infection. Specific antibody-producing capabilities of previously infected, trypanoicidal drug-treated voles were found to be comparable to uninfected controls, within 3 days following chemotherapy. Cell-mediated hypersensitivity responses to oxazolone were also significantly depressed by trypanosome infection; responses to the initial sensitization of oxazolone and to secondary challenge treatments were depressed compared to uninfected controls. Possible mechanisms of trypanosome-induced immunodepression are discussed.
The African trypanosome (Trypanosoma brucei brucei) in its bloodstream phase has been found to possess rather unique surface properties. Results of lectin and iron colloid binding studies have indicated that the parasite's surface coat is devoid of many types of exposed carbohydrate residues which commonly are expressed on a variety of mammalian cell types. These include: glucose, mannose, galactose, n-acetylglucosamine, n-acetylgalactosamine, and neuraminic acid. A number of these carbohydrates (E.G., glucose, mannose, galactose and n-acetylgalactosamine) are, however, buried within the surface coat as evidenced by lectin binding to trypsinized parasites. The surface of well preserved parasites also lack exposed sialic acid and phospholipid moieties. Moribund parasites (or trypsinzed organisms) with altered surface coats were found to possess well defined phospholipid regions, but not negatively charged sialyl residues. Results presented tend to suggest that carbohydrates and phospholipids are not present in the outermost portion of the glycocalyx, thus exerting little or no influence on surface-mediated biological activities. However, the presence of such components on the plasmalemma is presumed to be structurally significant; especially during those developmental phases where the glycocalyx is absent, i.e., fly midgut phase.
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The pathways of short-term tryptophan metabolism in rats infected with Trypanosoma brucei gambiense were studied to determine whether this amino acid undergoes rapid conversion to tryptophol and indole lactic acid, two metabolites produced in vitro by T. brucei gambiense. Intravenously administered L-(3-14-C)-tryptophan was metabolized to at least two compounds in infected rats: tryptophol (indole ethanol) and indole acetic acid. Indole lactic acid was not detected as a metabolite. Approximately 76 percent of the labeled substrate was metabolized along these pathways in 30 min. Control rats exhibited no detectable metabolism of tryptophan during the same period. These results indicate that dietary tryptophan may be diverted from the kynurenine and serotonin pathways by parasite metabolism to compounds possessing potential pharmacological or toxic activity.
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