Pseudomonas aeruginosa is an opportunistic pathogen that is an important cause of hospital-acquired infections. Despite constant exposure to this pathogen, healthy individuals do not get infected. In the setting of injured epithelium or immunocompromised host, however, P. aeruginosa is able to colonize and can cause devastating diseases in burn patients, patients on respiratory ventilators, contact lens wearers, cancer and AIDS patients, diabetic foot ulcer, and is one of the major causes of death in patients afflicted with cystic fibrosis. This highlights the importance of continued research on this pathogen in order to further our understanding of its mechanisms of infection and to develop effective means to combat and manage the diseases caused by it. P. aeruginosa is the epitome of an opportunistic pathogen of humans. P. aeruginosa does not infect uncompromised tissues, yet there is hardly any tissue that this pathogen cannot infect if the tissue defences are compromised in some manner. A number of in vitro and ex vivo studies support the notion that injured epithelium (wound) is a preferred niche for P. aeruginosa infections. We have demonstrated that P. aeruginosa employs a variety of novel virulence strategies, including inhibition of cytokinesis and induction of cell death to inhibit wound healing and cause more damage both in vitro and in vivo.
Our lab is highly multidisciplinary in nature. We conduct projects that involve bacterial pathogenesis, cancer biology, and chronic wound healing. The primary reseach areas of our lab are: (i) to determine the virulence mechanisms that make Pseudomonas aeruginosa such a successful pathogen; (ii) to determine the eukaryotic host responses that are intended to control bacterial pathogen infections; (iii) to develop antibiotic-free approcahes to reduce surgical site infections; and (iv) to employ bacterial toxins as molecular tools to dissect important mammalian cellular processes such as cytokinesis, cell cycle, apoptotic program cell death, and apoptotic compensatory proliferation signalling. We are actively conducting research in the following general areas:
This movie shows apoptotic compensatory proliferation signaling whereby a dying cell (green) releases a vesicle that stimulates proliferation in a bystander cells upon contact.
Our approach is multipronged and multidisciplinary in nature. We use leading-edge technology, including time-lapse videomicroscopy, stable cell lines and animal modeling, to carry out research in our laboratory.
(Left to right) Sasha Shafikhani, PhD; Amber Kaminski; Janet Zayas; Kajal Gupta, PhD; Douglas Gilbert; Joe Goldufsky, PhD
Current lab members |
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Anahita Aboonabi, PhD, postdoctoral fellow Email: Anahita_Aboonabi@rush.edu |
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Mohamed F. Mohamed, PhD, postdoctoral fellow |
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K A Foyez Mahmud, PhD, postdoctoral fellow Email: KAFoyez_Mahmud@rush.edu |
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Kaylee Delgado, graduate student Email: Kaylee_Delgado@rush.edu |
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Former lab members |
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Kajal Gupta | ![]() |
Ruchi Roy |
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Douglas Gilbert | ![]() |
Janet Zayas, PhD | ![]() |
Stephen Wood, PhD |
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Joe Goldufsky, PhD | ![]() |
Amber Kaminski, MS | ![]() |
Sasha Shafikhani, PhD
Rush University Department of Internal Medicine and the Rush Cancer Center
Phone: (312) 942-1368
Fax: (312) 942-2808
Email: sasha_shafikhani@rush.edu