Suppressed rejection of Trichinella spiralis in immunized rats concurrently infected with Eimeria nieschulzi.

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. Information in the literature showed that rodent hosts infected with such nematodes as Nippostrongylus brasiliensis and Ancylostoma caninum, or with certain bacterial species, such as Salmonella typhimurium, were more resistant to primary infection with Trichinella spiralis than were their unparasitized counterparts (Brewer, 1955; Cox, 1952; Louch, 1962). Resistance to a secondary infection with T. spiralis in mice also was enhanced when the host was infected with A. caninunm prior to challenge (Cox, 1952). Collectively, these findings are compatible with the premise that resistance to T. spiralis might be due to adverse changes in the parasite's environment (Larsh and Race, 1975). Such changes may be induced by inflammation caused by the priorestablished pathogens. Inflammation, as reflected by mucosal peroxidase activity and granulocyte infiltration of Received for publication 22 March 1977. * Work supported by Research Grant AM-11361 from the NIAID, National Institutes of Health. Dr. Castro is the recipient of Research Career Development Award AI-00087. t Department of Biology, The University of New Mexico, Albuquerque, New Mexico 87131. + Department of Physiology, University of Texas Medical School, Houston, Texas 77025. 83 the lamina propria, has been correlated positively with temporal and spatial distribution of T. spiralis in the small intestine of rats with primary trichinosis (Smith and Castro, 1975, 1977). Challenge infections in immunized rats were associated with a significant rise in peroxidase activity as early as day 2 postchallenge (Russell and Castro, 1977). In a similar but unrelated study we noted a decrease in mucosal peroxidase activity when rats were infected with an intracellular protozoan, Eimeria nieschulzi. These observations stimulated the present investigation. We hypothesized that if acquired resistance to T. spiralis was directly related to the level of mucosal inflammation, E. nieschulzi, unlike other enteric parasites studied, might have a suppressive effect on the immune response. The following is a description of the initial experiment on which our hypothesis was based and of subsequent experiments designed specifically to test our