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Immune responses associated with Eimeria papillata infections in mice

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Title: Immune responses associated with Eimeria papillata infections in mice
Author: Schito, Marco Larry
Department: Department of Pathobiology
Advisor: Barta, J.R.
Abstract: Eimerian parasites infect a wide range of economically important hosts including poultry, cattle and swine. These parasites cause coccidiosis, a disease that produces an enteritis characterized by reduced rate of weight gain and/or decreased egg production. The use of murine Eimeria species as a laboratory model for livestock coccidiosis has permitted the understanding of host's immune response towards the parasite. This thesis demonstrates that Eimeria papillata differs from most eimerian infections in mice since T lymphocyte mediated suppression of parasite replication was not found. Innate responses are responsible in limiting primary E. papillata infections while T cells mediate immunity against re-infection. During primary infections, natural killer cell produced IFN-$\gamma$ and neutrophil-mediated responses control parasite replication while B cells increase in the mesenteric lymph nodes. During patent primary infections isolated lymphocytes do not proliferate in response to mitogens or E. papillata parasite antigens, cytokine responses are skewed toward a TH-2 type and T cell activation markers do not differ from control. This immunosuppression is nitric oxide independent and may result from cross reactive parasite antigens present within parasite infected host cells. Immunity to re-infection appears to be T-cell-dependent and IFN-$\gamma$ independent. Cytokine responses in the mesenteric lymph node are minimal with the exception of interleukin-2 which is produced earlier and at higher quantities than in primary infections. Using immunofluorescent microscopy, higher numbers of $\alpha\beta\sp+$ TcR CD8$\sp+$ T cells appear in the intestinal tract coincident with immunity. However using mutant knockout mice, $\alpha\beta\sp+$ TcR CD4$\sp+$ T cells appear to play a major role while $\alpha\beta\sp+$ TcR CD8$\sp+$ T cells and perforin appear to play minor roles in controlling parasite replication. Lymphocytes may not be the only cells responsible for immunity. The transfer of mesenteric lymph node and intraepithelial lymphocytes from naive or previously infected BALB/c mice to recipient SCID mice do not significantly inhibit parasite replication. However, a protective response, as measured by significant reduction in oocyst output, was observed if SCID recipient mice were previously infected. This suggests that (a) the intestinal tract required a previous exposure possibly to express appropriate adhesion molecules for donor lymphocytes to traffic to the organ, or that (b) other cells within the gastrointestinal tract, in association with immune lymphocytes, play a role in mediating an effective host response towards E. papillata.
Date: 1997
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