PIPages
Labs

Jonathan Allen

Loyola University Chicago, IL·Microbiology & Immunology

*Pseudomonas aeruginosa* is one of the leading causes of infections acquired in hospitals, and high-risk strains are spreading as antibiotic resistance climbs and strains pick up new traits that make them more dangerous. With fewer drugs that still work, a practical route forward is to understand exactly how the most aggressive clinical strains cause disease, so that those mechanisms themselves become drug targets.

Fields

Microbiology & Immunology

Biology

Medicine & Clinical Research

Topics

Pseudomonas aeruginosa

healthcare-acquired infection

antibiotic resistance

Grants
1 known grant, through May 2027

What they work on

  1. Define at the molecular level how the CdiA toxin domain of Pseudomonas aeruginosa cleaves transfer RNA, the molecule that supplies amino acids during protein synthesis, in both bacterial and eukaryotic substrates.
  2. Determine the cellular consequences of CdiA toxin delivery into eukaryotic host cells and test whether the observed cytopathic effects depend on its tRNA-cleaving activity.
  3. Test the hypothesis that P. aeruginosa uses CdiA to intoxicate host cells and overcome barriers to infection, comparing wild-type and toxin-inactivating mutant strains in a mouse infection model.
  4. Build on comparative genomics of 100 clinical P. aeruginosa isolates linking accessory-genome genes to virulence in mice, to establish the contribution of contact-dependent growth inhibition genes to pathogenicity.

More about the research

Work in this lab aims to identify the strategies that make *P. aeruginosa* more virulent.

Why it matters

Pseudomonas aeruginosa infections are a worldwide public health problem, and rising antibiotic resistance leaves few treatment options for severe, invasive disease. Showing that the CdiA toxin delivery system helps the bacterium overcome host barriers would mark it as a target for drugs designed to disarm the pathogen and let the immune system clear the infection, rather than relying on conventional antibiotics.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Contribution of CdiA to Pseudomonas aeruginosa pathobiology

NIH · Jun 2021 – May 2027

Closest labs

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Juliane Bubeck Wardenburg

Washington University in St Louis, MO·Microbiology & Immunology

Determine how S. aureus alpha-toxin (Hla) impairs antigen-specific CD4+ T cells in skin infection, examining antigen trafficking, T-cell receptor signaling during infection, and whether T-cell ADAM10 levels predict susceptibility, using cell-type-specific transgenic mice and a human biorepository.

Stephen Dolan

Clemson University, SC·Microbiology & Immunology·Early-career

Define the molecular basis of communication between Aspergillus fumigatus and Pseudomonas aeruginosa, mediated by the toxins gliotoxin and hydrogen cyanide, by co-culturing them in synthetic cystic fibrosis sputum.

The school

Loyola University Chicago: 8 labs on PI Pages, $61M a year on research, 156 research doctorates a year.

More about Loyola University Chicago

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