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Bacteriology

Our research in bacteriology focuses primarily on the analysis of microbe-host interactions and antibiotic resistance. The department faculty study mechanisms underlying bacterial pathogenesis in diverse species, including pathogenic Legionella, Neisseria, Pseudomonas and Vibrio species. Work from the bacteriology laboratories has provided novel insights into bacterial-host cell interactions including attachment, mechanisms of metal acquisition by pathogens, structure and function of secreted toxins and effectors of virulence, the regulation of virulence factor expression, molecular changes that underlie key evolutionary transitions and the influence of DNA structure on gene expression, and mechanisms of antibiotic resistance, particularly those linked to ribosome function.

Labs in This Research Area

 Nicholas Cianciotto Lab

Pathogenesis of Legionella pneumophila and Stenotrophomonas maltophilia

Research Description

L. pneumophila, the agent of Legionnaires' disease, is a classic environmental, opportunistic pathogen. The aim of our research is to characterize the bacterial genes and gene products that promote the occurrence of Legionnaires' disease.

S. maltophilia is an environmental gram-negative bacterium that is being increasingly associated with an array of human infections, including most notably pneumonia. The emergence of S. maltophilia as a significant health concern is due in part to its marked antibiotic resistance. Our lab has developed murine models of lung infection and is currently identifying virulence factors produced by this important new pathogen.

We employ a multi-faceted approach toward understanding the pathogenesis and natural history of bacterial infectious disease, with the hope that basic insights will lead to new methods of disease prevention, diagnosis, or treatment.

For lab information and more, see Dr. Cianciotto’s faculty profile and lab website.

Publications

See Dr. Cianciotto's publications on PubMed.

Contact

Contact Dr. Cianciotto at 312-503-0385 or the lab at 312-503-1034.

Postdoctoral Fellow: Joshua Mayoral

Graduate Students: Carlton Adams, Armando BarajasBrandi CobeAlberto Lopez

Technical Staff: Alexis Vargas

 Alan Hauser Lab

Pathogenesis of Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae infections

Research Description

Our laboratory investigates the pathogenesis of the gram-negative bacteria Pseudomonas aeruginosa, Acinetobacter baumannii and Klebsiella pneumoniae. We focus on virulence factors such as the type III secretion, an apparatus that injects toxins directly into host cells. A second interest is the use of genomic approaches for the identification of novel virulence determinants. Our studies utilize a broad range of techniques, including molecular and cellular assays as well as animal models and epidemiologic studies on human populations.

For lab information and more, see Dr. Hauser's faculty profile and lab website.

Publications

See Dr. Hauser's publications on PubMed.

Contact

Contact Dr. Hauser at 312-503-1044 or the lab at 312-503-1081.

Faculty Collaborators: Kelly Bachta, Larry Kociolek, Egon Ozer

Postdoctoral Fellows: Jiwasmika Baishya, Thomas Bolig, Preeti Garai

Graduate Students: Bettina Cheung, Marine Lebrun Corbin, Grayce Mores, Claudia Oropeza, Aliki Valdes

Lab Manager: Sophia Nozick

Undergraduate Student: Christopher Axline

Research Staff: Arghavan Alisoltanidehkordi

 Karla Satchell Lab

Role of bacterial protein toxins in the pathogenesis of Vibrio vulnificus and Vibrio cholerae

Research Description

My research focuses on the role of secreted protein toxins on bacterial pathogenesis. The toxins we study are members of the MARTX family and are produced by Vibrio cholerae, a pathogen important for the diarrheal disease cholera, and Vibrio vulnificus, a pathogen that causes septicemia and necrotizing fasciitis from seafood consumption as well as wound infections. Our group studies the mechanism of action of these toxins using a combination of cell biology, biochemistry, and structural biology. In addition, we investigate the role of these toxins in pathogenesis using animal and tissue culture models with focus on mechanisms of tissue damage and evasion of innate immune clearance.

For lab information and more, see Dr. Satchell's faculty profile.

Publications

See Dr. Satchell's publications on PubMed.

Contact

Contact Dr. Satchell at 312-503-2162 or the lab at 312-503-1503.

Research Faculty: George Minasov, Ludmilla Shuvalova

Research Associate: Alfa Herrera

Research Project Manager: Nicole Inniss

Postdoctoral Fellows: Shantanu Shukla

Graduate Students: Caleb Stubbs

Technical Staff: Grant Wiersum

 Hank Seifert Lab

Bacterial pathogenesis, DNA recombination mechanisms, epithelial cell adherence

Research Description

Our laboratory studies the pathogenesis of Neisseria gonorrhoeae, the causative agent of the sexually transmitted disease gonorrhea. This gram-negative bacterium is an obligate human pathogen that has existed within human populations throughout recorded history. We are using a variety of molecular biological, genetic, cell biological and biochemical techniques to investigate the molecular mechanisms controlling gonococcal infection, define mechanisms and pathways of DNA recombination, replication and repair in this human specific pathogen, study the interactions between gonococci and human cells, tissues and the innate immune system and determine how the pilus functions to help mediate genetic transfer and pathogenesis. Our goal is to discover new mechanisms important for the continued existence of this microbe in the human population to further our understanding of how infectious agents have evolved to specifically infect humans.

For lab information and more, see Dr. Seifert's faculty profile.

Publications

See Dr. Seifert's publications on PubMed.

Contact

Contact Dr. Seifert at 312-503-9788 or the lab at 312-503-9786.

Research Faculty: Linda I-Lin Hu

Postdoctoral Fellows: Iryna BoikoJayaram Narayana, Kathleen Nicholson, Selma Metaane

Graduate Students: Wendy Geslewitz

Technical Staff: Kabita Kunwar, Clarence Sanders, Shaohui Yin

 M.-N. Frances Yap Lab

Molecular mechanisms of ribosome hibernation and antibiotic resistance

Research Description

We broadly investigate the mechanisms used in bacterial cells to regulate antibiotic resistance and gene expression at the translational level. Our long-term goals are to address mechanistic questions about ribosome specialization and resistance evolution, in addition to developing aptamer-based diagnostic tools for bacterial pathogens.

Multidrug resistant ribosome: Macrolides, lincosamides and streptogramins (MLS) are structurally distinct and broad-spectrum antibiotics that inhibit protein biosynthesis by binding to the 50S large subunit of bacterial ribosome.The efficacy of MLS has rapidly eroded due to the widespread dissemination of the Erm RNA methyltransferases that catalyze the transfer of two methyl groups to a conserved adenine nucleotide (m26A2058) in the 23S rRNA of the 50S subunit. This dimethylation sterically hinders the binding of all MLS antibiotics that share the overlapping A2058, in addition to abrogating the MLS resistant bacteria from host immune recognition. Our studies seek to addresses several unresolved questions: How is the expression of erm regulated under antibiotic selection? How does Erm find its target? What are the consequences of ribosome methylation? How do the next-generation antibiotics recognize the methylated ribosome?

Hibernating ribosome: The bacterial 100S ribosome (dimer of 70S complexes) is important for pathogenesis, translational repression, starvation responses, and ribosome turnover. Our goal is to establish a mechanistic understanding of the biogenesis and function of the 100S ribosome in translational silencing and staphylococcal pathogenesis. This project focuses on the following unexplored questions: What factors control the constitutive production of the 100S ribosome in S. aureus? Why are only specific mRNAs translationally repressed during ribosome hibernation? How is hibernation beneficial to ribosome stability? How is ribosome turnover linked to successful host colonization? These questions will be addressed through a multi-disciplinary approach that spans genetics, molecular biophysics, biochemistry and whole animal infection studies.

For lab information and more, see Dr. Yap's faculty profile and lab website.

Publications

See Dr. Yap's publications on ORCID.

Contact

Contact Dr. Yap.

Postdoctoral Fellows: Satpal Chodha, Alexandre Le Scornet, Anna Lipońska, David Ranava