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Georgia Veterinary Scholars Program at the UGA College of Veterinary Medicine

Georgia Veterinary Scholars Program

GVSP Summer 2009 Scholars


Georgia Veterinary Scholar

Faculty Mentor

Melissa Dugan

Melissa Dugan
University of Georgia
Class of 2012

Dr. Kaori Sakamoto
Dr. Sakamoto's Lab

UGA College of Veterinary Medicine

 

The Potential Role of the Adhesion Molecule CD18 in Cytauxzoonosis Pathogenesis
* M. Dugan, K. Frontera-Acevedo, L. Sellers, and K. Sakamoto


Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

Cytauxzoonosis is a fatal, incurable, emerging infectious disease of domestic cats caused by the protozoan parasite, Cytauxzoon felis.  Infection of monocytes leads to systemic illness and adhesion of the infected leukocytes to the endothelium of blood vessels, potentially occluding them.   The goal of this project was to characterize the feline immune response during cytauxzoonosis.  Clinically ill, C. felis-infected cats had elevated serum levels of the pro-inflammatory cytokines, TNF-a, IL-6, and IL-1b, as compared to healthy cats.  Immunocytochemistry of blood smears from C. felis-infected cats showed staining for IgM on the surface of erythrocytes that was not present in healthy control smears or with the use of isotype control antibodies.  We hypothesize that: 1) there is increased expression of the adhesion molecule, CD18, on infected monocytes in C. felis- infected cats, and 2) that this increased expression is important in disease pathogenesis.  To test the first part of this hypothesis, we performed immunohistochemistry for CD18 expression on lung tissues harvested from both healthy and C. felis-infected cats.  Increased CD18 staining was present on the surface of interstitial leukocytes, as well as intravascular monocytes, in C. felis-infected cats, whereas CD18 was only observed on alveolar macrophages in healthy control lung.  To test the second part, we used antibodies to neutralize CD18 on peripheral blood leukocytes from C. felis-infected cats, which resulted in the inhibition of pro-inflammatory cytokine responses to further stimulation with lipopolysaccharide.  We believe that anti-CD18 therapy could be used to prevent cytokine storms in critically ill cats with cytauxzoonosis.