Judith A. Whittum-Hudson, Ph.D. is an immunologist with long term research interests in the immunopathogenesis of infectious diseases and anti-chlamydial vaccine development. She has developed murine ocular infection models to study herpes simplex virus infections of the retina and brain and to study chlamydial infections of the conjunctiva. In both systems, the role of immune responses in protective vs pathogenic processes have been studied. With the ocular chlamydial infection model, Dr. Whittum-Hudson and colleagues discovered a protective, genus-specific anti-chlamydial vaccine which has now been shown to be protective against murine genital infection. The mechanisms of protective immunity which the vaccine induce are under active investigation in Dr. Whittum-Hudson's laboratory. .

After either ocular or genital chlamydial infections in mice, Dr. Whittum-Hudson has shown that organism can disseminate to joints of mice, suggesting that these animal models resemble some features of human chlamydia-associated reactive arthritis. In particular, the models may provide tools to study the initiating events in the pathogenesis of reactive arthritis (eg, the time when organism first arrives in synovial tissues to elicit important host inflammatory and immune responses). The key immunologic and microbiologic elements of this form of reactive arthritis are under study in both mouse models and patient samples, in collaboration with other faculty at Wayne State. Results from the human studies have guided some questions being asked in mouse models, but the inbred mouse models allow the testing of important questions impossible to address in human patients. The vaccine has been shown to reduce the synovial tissue inflammation seen after genital infection, suggesting that vaccination would reduce dissemination of organism. This is an important issue as other chlamydial species also disseminate, including C psittaci and C pneumoniae. Dr. Whittum-Hudson is also involved in collaborative studies of Chlamydia pneumoniae and its role in the pathogenesis of late-onset Alzheimer's Disease, as well as in molecular mimicry in causing EAE in rats, a model of multiple sclerosis.