Trypanosome-induced modulation of responses to concurrent helminth infection.

Infections with African trypanosomes are known to suppress immune responses to vaccines and to gastrointestinal nematode infections in livestock. Experimental infections with Trypanosoma brucei (Tb) and the gastrointestinal nematode Nippostrongylus brasiliensis (Nb) in mice were used to identify possible mechanisms involved in interference with anti-worm responses and to examine the effects of host genotype on the extent of suppression seen. Concurrent infections with T. brucei resulted in a prolongation of worm survival and a dramatic increase in faecal egg output. Infection also resulted in a marked suppression of the proliferative response of mesenteric lymphocytes (MLNC) to in vitro mitogenic stimulation. When MLNC from concurrently infected mice were stimulated in vitro with the mitogen ConA they released more IFN-gamma and less IL-5 than cells from mice infected only with N. brasiliensis. These data are interpreted in terms of a trypanosome-mediated influence on the development of host-protective type-2 T helper cell responses against N. brasiliensis. The degree to which T. brucei altered the kinetics of the nematode infection was influenced by the particular mouse strain concerned.