Joseph P. Vogel, PhD

Associate Professor
Molecular Microbiology

Molecular Microbiology and Microbial Pathogenesis Program
Plant and Microbial Biosciences Program
Molecular Cell Biology Program
Molecular Genetics and Genomics Program

  • 314-747-1029

  • 314-747-1030

  • 314-362-1232

  • 10220 McDonnell Pediatric Research Building



  • bacteriology, pathogenesis, macrophage, intracellular trafficking, immunology

  • Intracellular replication of Legionella pneumophila within macrophages

Research Abstract:

My laboratory is interested in how pathogens are able to survive and replicate inside host cells. We have chosen to focus on one bacterial pathogen, Legionella pneumophila, that is able to grow inside the hostile environment of professional phagocytic cells such as macrophages and fresh water amoebae. Growth of L. pneumophila inside alveolar macrophages of the human lung results in a potentially fatal form of pneumonia called Legionnaires’ disease. L. pneumophila is able to survive inside host cells by preventing fusion of the nascent phagosome with the degradative compartment, the lysosome.

We have discovered a large number of L. pneumophila genes that are absolutely required for intracellular replication. These genes are called “dot” for defect in organelle trafficking because mutant strains lacking these genes are unable to perturb the normal endocytic pathway of the macrophage. Based on similarities between the dot genes and bacterial conjugation systems, we believe that the dot machine constitutes an export apparatus that evolved from a plasmid transfer system. The dot secretion complex presumably is used to deposit virulence factor(s) into host cells that are then responsible for preventing phagosome-lysosome fusion. In addition to L. pneumophila, a number of other pathogens including Bordetella pertussis, Helicobacter pylori, and Brucella abortus contain related complexes which have all been classified as type IV secretion systems. Determining how these specialized export apparatuses function will allow us to understand how these pathogens cause disease and reveal methods to prevent or inhibit their action.

Selected Publications:

Jeong KC, Sexton JA, Vogel JP. 2015. Spatiotemporal regulation of a Legionella pneumophila T4SS substrate by the metaeffector SidJ. PLoS Pathog. e1004695. PMCID: PMC4361747.

Jeong KC, Sutherland MC, Vogel JP. 2015. Novel export control of a Legionella Dot/Icm substrate is mediated by dual, independent signal sequences. Mol. Microbiol. 96(1):175-88. PMID: 25582583.

Chole RA, Gagnon PM, Vogel JP. 2014. Inactivation of specific Pseudomonas aeruginosa biofilm factors does not alter virulence in infected cholesteatomas. Otol Neurotol. O35(9):1585-91. doi: 10.1097/MAO.0000000000000558.

Sutherland MC, Binder KA, Cualing PY, Vogel JP. 2013. Reassessing the role of DotF in the Legionella pneumophila type IV secretion system. PLoS One. 8(6):e65529. doi: 10.1371/journal.pone.0065529. PMID: 23762385.

Sutherland MC, Nguyen TL, Tseng V, Vogel JP. 2012. The Legionella IcmSW complex directly interacts with DotL to mediate translocation of adaptor-dependent substrates. PLoS Pathog. e1002910. PMCID: PMC3441705.

Vincent CD, Friedman JR, Jeong KC, Vogel JP. 2012. Identification of the DotL coupling protein subcomplex of the Legionella dot/icm type IV secretion system. Mol. Microbiol. 85:378-391. PMCID: PMC3391322.

Sutherland MC, Vogel JP. 2012. Reclamation of ampicillin sensitivity for the genetic manipulation of Legionella pneumophila. Appl Environ Microbiol. 78(15):5457-9. PMID: 22635996.

Vogel JP, Andrews HL, Wong SK, Isberg RR. 1998. Conjugative transfer by the virulence system of Legionella pneumophila. Science. 279(5352):873.

Last Updated: 6/1/2016 9:16:07 AM

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