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dc.contributor.advisorSterling, Charles R.en_US
dc.contributor.authorNovak, Susan Marie.
dc.creatorNovak, Susan Marie.en_US
dc.date.accessioned2011-10-31T17:41:38Z
dc.date.available2011-10-31T17:41:38Z
dc.date.issued1991en_US
dc.identifier.urihttp://hdl.handle.net/10150/185563
dc.description.abstractImmunohistochemical analysis of intestinal tissue from infected and uninfected neonatal mice was performed to determine immune responsiveness to Cryptosporidium parvum at the gut level. Infected mice showed a significant increase in T cell (T helper/T cytotoxic/suppressor) populations (p < 0.001), macrophages (p < 0.001), IL-2R positive cells (p < 0.001 at 16 days PI), and IgA positive cells (p < 0.001 at 16 days PI) compared to control (uninfected) animals. No differences between the two groups of animals existed for B cell populations of the IgG (p = 0.264) and IgM (p = 0.646) isotype. Cellular immunity seems to be primarily responsible for clearing cryptosporidial infection from infected animals. Humoral immunity mediated by B cells of the IgA isotype could be a secondary (delayed) factor which aids in the recovery of the animal. Neonatal mice were also infected with C. parvum to describe the susceptibility dynamics in this animal model. Percent infectivity of the animals (infected at various days of age beginning on day 4 and ending at day 18) began to decrease at 10 days of age (33% infectivity). Infectivity percentages varied up until 14 days of age and older when all of the animals inoculated were refractory to infection. Why this refractiveness to infection occurs as the animals age is still unknown. In another study neonatal mice infected at 4 days of age continued to be positive for parasites up until 25 days of age (21 days PI). Percent infectivity began to vary at 20 days of age (16 days PI) which meant that only a certain percentage of the mice tested at that time point were positive for C. parvum. Prior to 20 days of age 100% of the animals tested were infected. Proliferative responses of spleen cells from infected and control mice to C. parvum antigen were measured. Spleen cells from infected animals responsed to C. parvum antigen in vitro (stimulation index (SI) = 14.52 (infected mouse #1); 14.23 (infected mouse #2)) whereas cells from uninfected mice did not (SI = 1.12 (control mouse #1); 1.07 (control mouse #2)). The spleen seems to be one organ involved in the immune circuitry responsible for clearance of cryptosporidiosis in neonatal mice.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.subjectDissertations, Academicen_US
dc.subjectMicrobiologyen_US
dc.subjectImmunology.en_US
dc.titleGastrointestinal cellular and humoral immune responses in BALB/c mice infected with Cryptosporidium parvum.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.identifier.oclc711706280en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.contributor.committeememberYocum, Daviden_US
dc.contributor.committeememberNagle, Rayen_US
dc.contributor.committeememberJoens, Lynnen_US
dc.contributor.committeememberHendrix, Maryen_US
dc.identifier.proquest9200016en_US
thesis.degree.disciplineMicrobiology and Immunologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.namePh.D.en_US
dc.description.noteThis item was digitized from a paper original and/or a microfilm copy. If you need higher-resolution images for any content in this item, please contact us at repository@u.library.arizona.edu.
dc.description.admin-noteOriginal file replaced with corrected file August 2023.
refterms.dateFOA2018-08-23T04:29:40Z
html.description.abstractImmunohistochemical analysis of intestinal tissue from infected and uninfected neonatal mice was performed to determine immune responsiveness to Cryptosporidium parvum at the gut level. Infected mice showed a significant increase in T cell (T helper/T cytotoxic/suppressor) populations (p < 0.001), macrophages (p < 0.001), IL-2R positive cells (p < 0.001 at 16 days PI), and IgA positive cells (p < 0.001 at 16 days PI) compared to control (uninfected) animals. No differences between the two groups of animals existed for B cell populations of the IgG (p = 0.264) and IgM (p = 0.646) isotype. Cellular immunity seems to be primarily responsible for clearing cryptosporidial infection from infected animals. Humoral immunity mediated by B cells of the IgA isotype could be a secondary (delayed) factor which aids in the recovery of the animal. Neonatal mice were also infected with C. parvum to describe the susceptibility dynamics in this animal model. Percent infectivity of the animals (infected at various days of age beginning on day 4 and ending at day 18) began to decrease at 10 days of age (33% infectivity). Infectivity percentages varied up until 14 days of age and older when all of the animals inoculated were refractory to infection. Why this refractiveness to infection occurs as the animals age is still unknown. In another study neonatal mice infected at 4 days of age continued to be positive for parasites up until 25 days of age (21 days PI). Percent infectivity began to vary at 20 days of age (16 days PI) which meant that only a certain percentage of the mice tested at that time point were positive for C. parvum. Prior to 20 days of age 100% of the animals tested were infected. Proliferative responses of spleen cells from infected and control mice to C. parvum antigen were measured. Spleen cells from infected animals responsed to C. parvum antigen in vitro (stimulation index (SI) = 14.52 (infected mouse #1); 14.23 (infected mouse #2)) whereas cells from uninfected mice did not (SI = 1.12 (control mouse #1); 1.07 (control mouse #2)). The spleen seems to be one organ involved in the immune circuitry responsible for clearance of cryptosporidiosis in neonatal mice.


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