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dc.contributor.authorShahbazian, Lotfollah Masoud.
dc.creatorShahbazian, Lotfollah Masoud.en_US
dc.date.accessioned2011-10-31T18:13:41Z
dc.date.available2011-10-31T18:13:41Z
dc.date.issued1993en_US
dc.identifier.urihttp://hdl.handle.net/10150/186594
dc.description.abstractA murine model of acquired immunodeficiency syndrome (AIDS) was developed by infecting C57BL/6 mice with murine leukemia retrovirus LP-BM5. Murine AIDS shares many features with human AIDS. Murine and human AIDS cause impairment of cell-mediated and humoral immune responses, and increase risk of opportunistic infection such as Streptococcus pneumoniae. Cofactors such as ethanol may determine the severity of the retrovirus infection and the rate of progression to AIDS. Changes in nutritional status due to retrovirus infection or ethanol consumption, can play an important role in immunomodulation in the animal. Immunomodulation observed in animals with chronic ethanol ingestion is associated with age of the animal, the nutritional composition of the diet, and the amount of ethanol consumed. Young mice are more sensitive to the immunomodulating effects of ethanol and diet than mature mice. The percentage of B cells in mature mice was significantly increased with consumption of nutritionally superoptimal diet containing ethanol while ethanol ingestion with a nutritionally inadequate diet severely decreased the percentage of B cells when compared to control or pair-feeding. Cytokine secretion, and natural killer cell and phagocytic activities were modulated by ethanol as well as by the nutritional quality of the diet. Both retrovirus infection and ethanol consumption affected survival rate after Streptococcus pneumoniae infection in mice. Chronic ethanol consumption, but not retrovirus infection resulted in significant reduction in serum level of anti pneumococcal polysaccharide antibody which in combination with complement system make up an important part of host defense against S. pneumoniae. However, retrovirus infection significantly reduced resistance to S. pneumoniae. Retrovirus infected mice fed a diet containing a high concentration of ethanol for short term exhibited a greater resistance to S. pneumoniae infection than mice fed diets with low concentration or no ethanol. S. pneumoniae antigen immunization improved survival of the mice infected with S. pneumoniae. In conclusion, ethanol and nutritional adequacy of diet induced immunomodulation of the host. Ethanol consumption during retroviral infection may accelerate the progression of murine AIDS through changes in the lymphoid cells and resistance to S. pneumoniae infection.
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, Academic.en_US
dc.subjectNutrition.en_US
dc.subjectImmunology.en_US
dc.titleDietary ethanol modulates immune responses, and alter resistance to Streptococcus pneumoniae in LP-BM5 retrovirus infected mice.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.contributor.chairWatson, Ronald R.en_US
dc.identifier.oclc722392543en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.contributor.committeememberEarnest, David L.en_US
dc.contributor.committeememberGerba, Charles P.en_US
dc.contributor.committeememberWeber, Charles W.en_US
dc.identifier.proquest9422819en_US
thesis.degree.disciplineNutritional Sciencesen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.namePh.D.en_US
refterms.dateFOA2018-04-25T21:14:01Z
html.description.abstractA murine model of acquired immunodeficiency syndrome (AIDS) was developed by infecting C57BL/6 mice with murine leukemia retrovirus LP-BM5. Murine AIDS shares many features with human AIDS. Murine and human AIDS cause impairment of cell-mediated and humoral immune responses, and increase risk of opportunistic infection such as Streptococcus pneumoniae. Cofactors such as ethanol may determine the severity of the retrovirus infection and the rate of progression to AIDS. Changes in nutritional status due to retrovirus infection or ethanol consumption, can play an important role in immunomodulation in the animal. Immunomodulation observed in animals with chronic ethanol ingestion is associated with age of the animal, the nutritional composition of the diet, and the amount of ethanol consumed. Young mice are more sensitive to the immunomodulating effects of ethanol and diet than mature mice. The percentage of B cells in mature mice was significantly increased with consumption of nutritionally superoptimal diet containing ethanol while ethanol ingestion with a nutritionally inadequate diet severely decreased the percentage of B cells when compared to control or pair-feeding. Cytokine secretion, and natural killer cell and phagocytic activities were modulated by ethanol as well as by the nutritional quality of the diet. Both retrovirus infection and ethanol consumption affected survival rate after Streptococcus pneumoniae infection in mice. Chronic ethanol consumption, but not retrovirus infection resulted in significant reduction in serum level of anti pneumococcal polysaccharide antibody which in combination with complement system make up an important part of host defense against S. pneumoniae. However, retrovirus infection significantly reduced resistance to S. pneumoniae. Retrovirus infected mice fed a diet containing a high concentration of ethanol for short term exhibited a greater resistance to S. pneumoniae infection than mice fed diets with low concentration or no ethanol. S. pneumoniae antigen immunization improved survival of the mice infected with S. pneumoniae. In conclusion, ethanol and nutritional adequacy of diet induced immunomodulation of the host. Ethanol consumption during retroviral infection may accelerate the progression of murine AIDS through changes in the lymphoid cells and resistance to S. pneumoniae infection.


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