While infection with parasitic helminths remains a major concern for a quarter of the worlds’ population in non-westernized societies, the incidence of infection has significantly reduced in westernized societies. Simultaneously, the incidence of autoimmune diseases, such as inflammatory bowel disease, is on the rise in the industrialized-west. Studies of infection with various helminths, including the rat tapeworm, Hymenolepis diminuta, in murine models of inflammatory disease reveal the potential of helminth-based therapeutics. Serotonin (5-hydroxytryptamine, 5-HT) has previously been shown to be responsive to infection with a helminth. It has a variety of immunomodulatory actions in the gastrointestinal tract, yet its potential role in helminth expulsion and helminth therapy is largely unknown. Thus, the research presented in this thesis sought to test the hypothesis that infection with H. diminuta evokes increases in mucosal serotonin levels, important for fine-tuning type 2 (Th2) immunity and are involved in H. diminuta-mediated inhibition of dinitrobenzene sulphonic acid (DNBS)-induced colitis. Three specific aims were: (1) assess changes in murine intestinal serotonin following infection with H. diminuta, (2) determine if serotonin was important in the expulsion of H. diminuta from its non-permissive mouse host; and, (3) evaluate if manipulation of the enteric serotonergic system affected H. diminuta-evoked suppression of murine colitis caused by DNBS. This study did not find evidence of an increase in serotonin in the small intestine of H. diminuta-infected male BALB/c mice, and the extrinsic manipulation of the serotoninergic system via systemic delivery of a tryptophan hydroxylase inhibitor (para-chlorophenylalanine), 5-HT7 receptor antagonist (SB269970), or selective serotonin reuptake transporter inhibitor (fluoxetine) had negligible effects on worm expulsion or systemic Th2 events post-infection. Thus, the data do not support the hypothesis that enteric serotonin is a major influence of the immune response to infection with H. diminuta. Preliminary findings, however, suggest that the stress response to consecutive daily handling and i.p. injections may abrogate the helminth-evoked suppression of DNBS-induced colitis in mice, highlighting the neuro-immune axis and stress component of experimental design when studying inflammatory disorders.