My current research interests explore the mechanisms used by pathogenic bacteria to adapt to their host environment. Helicobacter pylori, a Gram negative pathogen that resides in the GI tract of its host, is able to persist for decades in the stomach without causing clinical symptoms. Previous studies suggest that H. pylori undergoes phase variation of Lewis antigens that are constituents of their LPS, and that this variation in Lewis antigen expression allows H. pylori to evade the immune system. The mechanisms that control Lewis antigen variation have not yet been characterized. H. pylori shows extensive genetic diversity between strains, and extensive intrahost genetic diversity also has been documented. We are interested in studying the sources of Lewis antigen diversity in H. pylori, concentrating on the genes directly involved in their synthesis pathways. Many of these genes possess regions in their sequences that could induce intragenomic recombination. We want to examine the function of genetic recombination on Lewis antigen diversity in H. pylori. Uncovering the means by which H. pylori is able to alter its Lewis antigenic structure would provide us insight into the disease processes induced by this bacterium.
| Sanabria-Valentin, Edgardo; Colbert, Marie-Teresa C; Blaser, Martin J (2007) Role of futC slipped strand mispairing in Helicobacter pylori Lewisy phase variation. Microbes Infect 9:1553-60 |
