Northwestern University Feinberg School of Medicine

Center for Genetic Medicine

Wyndham W Lathem, PhD

Wyndham W Lathem, PhD

Associate Professor of Microbiology-Immunology



Ward Building Room 3-307
303 E Chicago Avenue
Chicago IL 60611

lathem( at )

Education/Research Website

Education and Certification

PhD: University of Wisconsin, Microbiology (2003)
Postdoctoral Fellowship: Washington University School of Medicine, Molecular Microbiology (2007)


Description of Interests

Yersinia pestis and Yersinia pseudotuberculosis are two bacterial pathogens that are very closely related, yet cause vastly different diseases in the mammalian host. Y. pestis is infamous for causing the devastating disease plague, while Y. pseudotuberculosis infection often results in a mild, self-limiting gastrointestinal illness. While genetically similar, the distinct mechanisms by which these two bacterial species interact with the host is of great interest to our group. Shared amongst both pathogens is a protein called Hfq, which serves as a chaperone for small, non-coding regulatory RNAs (sRNAs). One set of projects in the lab centers on understanding the post-transcriptional regulatory networks controlled by Hfq and sRNAs in both Yersinia species, particularly as they relate to virulence. Our group is testing the hypothesis that the similarities and differences in sRNA gene content and expression between these species may explain how a relatively mild pathogen evolved into one of the most deadly known to mankind. We are also interested in determining the mechanisms by which Y. pestis specifically causes primary pneumonic plague, a respiratory form of disease that Y. pseudotuberculosis does not produce. Therefore, another set of projects in the lab focuses on dissecting the mechanisms by which the Y. pestis virulence factor known as the plasminogen activator Pla, a bacterial cell surface-bound protease, controls the development of pneumonic plague. These include understanding the interaction of Y. pestis and Pla with the mammalian fibrinolytic and coagulation cascades, the identification of additional host substrates cleaved by Pla that lead to the development of a severe pneumonia, and the mechanisms by which Pla specifically induces an overwhelming inflammatory response in the lungs during infection.

Interests (Keywords)

Bacteriology; Gene Regulation; Genomics; Immunology; Infectious Diseases-bacteria; Inflammation; Microbial Pathogenesis; Respiratory Diseases

Research and Publications

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