Our laboratory studies the opportunistic bacterial pathogen Pseudomonas aeruginosa and its interaction with host cells at mucosal surfaces. The genome of P. aeruginosa contains a larger complement of regulatory genes than any other bacterial genome, reflecting the ability of P. aeruginosa to survive in a wide variety of environmental reservoirs and to successfully colonize and infect plant, insect and mammalian hosts. We are interested in discovering new regulatory pathways that control adaptation to the host and expression of virulence factors, in particular Type III secretion. In addition to protein-based regulatory systems, we are also studying small RNA-dependent regulation in this pathogen. The lab also studies the cell biology of host-pathogen interactions, and focuses on how Pseudomonas-epithelial cell interactions contribute to the establishment of an innate immune response during infection. Lastly, we have translational research projects that examine whether the presence of absence of virulence factors in clinical Pseudomonas isolates can be used to guide diagnosis and treatment of infection.

Kazmierczak BI, Jou TS, Mostov K, Engel JN. (2001) RhoGTPase activity modulates Pseudomonasaeruginosa internalization by epithelial cells. Cell Microbiol 3: 85-98.

Geiser TK, Kazmierczak BI, Garrity-Ryan LK, Matthay MA, Engel JN. (2001) Pseudomonasaeruginosa ExoT inhibits in vitro lung epithelial wound repair. Cell Microbiol 3: 223-226.

Kazmierczak BI, Engel JN. (2002) Pseudomonasaeruginosa ExoT acts in vivo as a GTPase activating protein for RhoA, Rac1 and Cdc42. Infect Immun 70: 2198-2205.

Kazmierczak BI, Mostov K, Engel JN. (2004) Epithelial cell polarity alters Rho-GTPase responses to Pseudomonasaeruginosa. Mol Biol Cell 15: 411-419.

Laskowski MA, Osborn E, Kazmierczak BI. (2004) A novel sensor kinase-response regulator hybrid regulates Type III secretion and is required for virulence in Pseudomonas aeruginosa. Mol Microbiol 54: 1090-1103.