This study deals with the effect of Eimeria nieschulzi infection on the host immune response to Trichinella spiralis. Six male Sprague-Dawley rats were inoculated with 10' and six with 10'; sporulated E. nieschulzi oocysts. On days 2, 8, and 16 postinoculation (PI), two rats from each infected group, and their paired uninfected controls, were killed and mucosal scrapings from their small intestines were assayed for peroxidase activity. Peroxidase levels were higher than corresponding control values on days 2 and 16 PI and significantly lower than the controls on day 8 PI. These data led us to initiate the present study because infection by T. spiralis in rats is known to cause an elevated gut peroxidase level which, in turn, is thought to contribute to worm expulsion. Twentyeight male rats were then immunized by administration of 7.5 X 103 freshly isolated T. spiralis larvae. Thirty-two days after immunization 16 rats were inoculated with 5 X 105 sporulated oocysts of E. nieschulzi. The other 12 rats were retained as immlune controls. Each of the 28 rats was challenged with 7.5 X 103 T. spiralis larvae between 2 and 10 days postinoculation with E. nieschulzi. Two or three coccidia-infected rats and two immune controls were killed at 2 and 5 days postchallenge with T. spiralis, and the worms in each third of the small intestine were recovered and counted. In every instance, rats that had concurrent coccidia infections harbored at least 4 times more T. spiralis than did immune, coccidia-free controls. Distribution of T. spiralis through the small bowel was not altered by infection with E. nieschulzi, despite the fact that the coccidian significantly suppressed worm rejection.
The possible direct role of inflammatory cells in resistance to Trichinella spiralis was studied by observing the effects of lamina propria cells from the small intestine (LP cells) of immunized rats on various stages of the parasite. Effects produced by physically disrupted cells were compared to those produced by intact cells on worms exposed to phytohemagglutinin or immune serum. LP cells were isolated from the rat intestine by collagenase digestion of everted gut segments that were previously denuded of epithelium by treatment with hyaluronidase. Disrupted cells, but not intact ones, selectively killed T. spiralis juvenile and adult worms in vitro, whereas larvae were unaffected by similar treatment. Attempts to identify the lethal component of disrupted cells led to an evaluation of the enzyme, peroxidase. Mucosal peroxidase is localized in LP cells and its activity increases several-fold during intestinal trichinosis. It is presumed to be myeloperoxidase, a particulate-bound enzyme of myeloid-derived leukocytes that functions as part of a potent antimicrobial system in combination with H2O2 and a halide. Results indicated that the vermicidal component of LP cells was associated with the pellet fraction of disrupted centrifuged LP cells, but was not linked to a peroxidase-H2O2-halide system.
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