The Erickson Lab

Our laboratory is focused on questions related to pathogen evolution, gene expression, and adaptation to different environments. We are especially interested in understanding how bacterial pathogens disrupt, avoid, or otherwise compromise the innate immune systems of their hosts. We primarily work with bacteria in the genus Yersinia, which includes Y. pestis, the cause of bubonic plague, as well as Y. pseudotuberculosis and Y. enterocolitica, which cause food-borne illnesses.

Some of the current research questions we are pursuing are:

1. How is biofilm production in Yersinia regulated?
Biofilm formation is a key factor in transmission of Y. pestis by fleas and may increase Y. pseudotuberculosis and Y. enterocolitica survival in the environment. We have characterized several regulatory genes that affect biofilms produced by these species.

2. What are the components of the insect innate immune system that affect Y. pestis growth?
Fleas transmit Y. pestis to susceptible mammals and the bacteria must adapt to both hosts. We have characterized the changes in gene expression that occur in fleas following infection and are investigating the role of specific immune defenses in establishing a transmissible infection.

3. How do Yersinia and other Gram-negative bacteria resist killing by anti-microbial chemokines?
Several chemokines are directly antimicrobial and are prevalent at mucosal sites where the bacteria colonize. We are investigating how specific bacterial genes affect chemokine binding and bacterial survival.

4. How do the normal bacterial residents in fleas affect the survival or transmission of Y. pestis?
Bacterial pathogens must not only overcome host defenses but also must co-exist with or eliminate complex microbial communities. We are characterizing the normal flora of fleas and how Y. pestis interacts with this community.

Y. pseudotuberculosis mutations that enhance biofilm formation also affect adsorption of Congo-red dye. Click to enlarge.
Xenopsylla cheopis fleas are able to limit Y. pestis infection to the midgut (dark area) through innate immune mechanisms yet to be discovered. Click to enlarge.
Mutant strains of Y. pseudotuberculosis differ from the wild-type strain in their affinity to antimicrobial chemokines, as measured by flow cytometry. Click to enlarge.
A mutation in the rfaD gene of Y. pseudotuberculosis enhances susceptibility to antimicrobial chemokine. Click to enlarge.
Sectioned midgut tissues from X. cheopis showing epithelial layer. Remnants of a recent blood meal and normal flora within the midgut lumen are visible. Click to enlarge.