Professor, Division of Human Biology
Professor, Public Health Sciences Division
Affiliate Professor, Basic Sciences Division
Affiliate  Professor, University of Washington Department of Microbiology

I am interested in how Helicobacter pylori adapts to the hostile and ever-changing environment of the host gastric epithelium. I use next-gen sequencing data to look at large, structural genetic polymorphisms that arise over chronic colonization. I characterize the functional effects of these polymorphisms using an array of molecular tools, proteomics, and microscopy.

I am investigating the innate immune response to H. pylori using both in vitro and in vivo models to better understand how infection with this pathogen leads to chronic inflammation.

I am interested in understanding the mechanisms H. pylori uses to adapt and persist within its human host during periods of chronic infection. To do this I take a functional genomics approach, using both next-gen sequence data to compare populations over time and basic genetic tools and techniques to identify specific factors that facilitate adaptation during chronic infection.

Along with making sure things run smoothly in the lab, I am also involved in many research projects. In particular I am interested in determining what genes are important for H. pylori colonization of the stomach, and what genes are necessary for its persistence. 

My research expertise is in chronic bacterial infections and their impact on the host. In the Salama lab I am using mouse models and human tissue samples to investigate the molecular mechanism(s) through which chronic Helicobacter pylori infection leads to the development of gastric cancer.

I am investigating how a cytoskeletal protein in H. pylori helps the bacteria maintain its characteristic helical cell shape and how this shape promotes pathogenesis. To understand how this protein defines H. pylori’s helical cell shape I use bacterial genetics, multiple types of microscopy, and biochemical techniques. Additionally, I use 2D gastric organoid models to understand how modulating the shape of H. pylori impacts its ability to colonize the gastric epithelium and cause disease.