Mechanisms for stochastic and tightly controlled regulation of Helicobacter pylori adhesins
The bacterium H. pylori colonizes the human stomach of more than half of the world's population. Among the infected, the majority remains non-symptomatic while a minor subpopulation develops severe gastric disease such as peptic ulcer of gastric cancer. Unless treated, H. pylori colonizes the harsh environ in the stomach for the lifetime. Adhesion of H. pylori to the gastric epithelial lining is a key factor for establishment of the lifelong persistent infection. The so far best-studied adhesin is the blood group antigen binding adhesin BabA, which mediate binding to ABO-blood group antigens present in the gastric epithelial lining. Another well-characterized adhesin is the sialic acid binding adhesin, SabA, which mediates binding to the sialyl-Lewis a/x antigens in inflamed gastric mucosa. We have in previous studies described mechanisms that affect adhesin-receptor interactions and in particular mechanisms that affect adhesin expression. With our expertise in H. pylori genetics in combination with biochemical approaches, we seek to continue to unravel the molecular mechanisms that operate to fine-tune expression of the BabA and the SabA adhesins in relation to environmental factors and disease.
H. pylori outer membrane vesicles (OMV) and host cellular responses
We are also interested in outer membrane vesicles that are shedded from the H. pylori bacterial surface, the function of vesicles as vehicles for delivery of bacterial virulence factors and the corresponding host cellular response.