Model of C. jejuni invasion of a host epithelial cell.
Campylobacter jejuni invasion of host cells is a multifactorial process, dependent on bacterial adhesins and effector proteins, as well as host cell signaling components. The surface exposed CadF and FlpA proteins allow C. jejuni to attach to host cells via binding fibronectin, a component of the extracellular matrix. The Cia proteins are secreted through the flagellar Type III Secretion System and delivered to the cytosol of the host cell. The coordinated actions of binding and Cia protein delivery result in activation of components of the focal complex, shown here in blue and yellow. Activation of these signaling components results in cytoskeletal rearrangements, leading to membrane ruffling and internalization of the bacteria.
Research & Interests
Campylobacter jejuni is one of the leading bacterial causes of human gastrointestinal disease worldwide. In 2011, the incidence of culture-confirmed C. jejuni infection was 14.31 cases/100,000 persons in the United States, the greatest incidence since 2000. Additional intervention strategies and treatments are needed to reduce the incidence and burden of C. jejuni disease.
The Konkel research group focuses on the characterization of host-C. jejuni interactions. Biochemistry, cell biology, molecular biology, and genomic/proteomic approaches are currently being used to understand the unique virulence factors that contribute to the pathogenesis of this facultative intracellular bacterium. We have one of the most comprehensive collection of C. jejuni strains in the world. One of our current aims is to identify and characterize cell binding and entry-promoting proteins used by C. jejuni to cause disease. To this extent, we have identified several novel virulence factors (please see our published manuscripts). Our model of C. jejuni binding and entry into host cells is shown below. We are extremely fortunate to work with some of the best scientists and research laboratories in the world.