Date of Defense

Spring 2-6-1998

Department

Biological Sciences

First Advisor

Leonard Beuving, Biological Sciences

Second Advisor

Robert Eversole, Biological Sciences

Third Advisor

John Jellies, Biological Sciences

Keywords

hormones

Abstract

Eosinophils are bone marrow derived granular leukocytes that play an important role in allergic reactions and a host immunological response to certain parasites. Recent findings suggest that the controlled expression of adhesion moleculres on different leukocyte subclasses and changes in the adhesive nature of activated endothelium serve as an antecedent event in the selective recruitment of different leukocytes. When these regulatory mechanisms that govern eosinophil activation and recruitment are altered the eosinophil may participate in the pathogenesis of disease such as asthma in the lung, Chron's disease in the gut, and atopic dermatitis in the skin. Estrogen treatment of the immature or ovariectomized rat uterus results in a massive influx of eosinophils into the endometrium. While this model of estrogen-mediated eosinophilia has been documented over the course of the past three decades, little has been uncovered as to the mechanisms that signal eosinophil migration to the uterus or how this migration profile compares to normal physiological, immunological, or pathological induced states of eosinophilia. We examined the effects of estrogen on the vascular adhesion profile of the ovariectomized rat uterus and the similarities between this model of estrogen induced eosinophilia and other models of migration described in the literature. In our study we have shown that ICAM-1 expressin of the vasculature and LFA-1 expression on eosinophils in the estrogen-treated uterus are down-regulaed in comparison to controls. Additionally, VCAM-1 is not expressed on either treated or control uteri which is consistent with our findings that VLA-4 is not expressed on the uterine eosinophil upon estrogen stimulation. This data may suggest an uncharacterized eosinophil specific adhesion pathway that does not rely on either LFA-1/ICAM-1 or VLA-4/VCAM.

Access Setting

Honors Thesis-Campus Only

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