Rahme Lab

Pseudomonas aeruginosa – a human opportunistic pathogen – is an extremely versatile microbe capable of infecting diverse hosts. To control disease development, it is pivotal to understand the pathogen’s strategies and the responses to them. Since my aim is to study this microbe’s interaction with the host, I am using Drosophila melanogaster as a model host, due to the advantages that it offers as a model system. Whole-genome expression study of the Drosophila transcriptome, following infection with virulent and avirulent P. aeruginosa strains, constitutes a rapid approach for pinpointing genes related to defense and virulence. Functional verification of the genes selected using this method is the second necessary step, in order to validate the huge amount of information that genome-wide expression analysis generate.

Arunava Bandyopadhaya, Ph.D. - Research Fellow
bandyopadhaya@molbio.mgh.harvard.edu

Arunava

Pseudomonas aeruginosa is a key opportunistic pathogen causing severe acute and chronic nasoconimial infections in immunocompromised or catheterized patients. I am interested on the molecular mechanisms of host-pathogen interaction to develop highly needed new strategies for prevention and therapy. To address this problem I am looking into small anti-infective compounds and the mechanisms through which they are altering the cellular and physiological changes in the immune system in mouse burn infection and lung infection model following Pseudomonas infection.

In bacteria, modulation and coordination of gene expression may occur as a result of population density via the regulated production of small molecules that serve as intricate signals that impact virulence gene expression. I am studying the P. aeruginosa MvfR regulon with the goal to understand how microbes translate these signals along with environmental signals to coordinate and modulate gene expression in order to adapt within different niches and overcome hostile environments. I employ high throughput screens, genetic and biochemical tools as well as various host models to study P. aeruginosa host interaction. My work has implications on both basic and applied research and I hope to contribute in the Lab effort to develop novel anti-infective drug therapies.

My work focuses on the identification and characterization of two novel pathogenicity islands of P. aeruginosa strain PA14. Pathogenicity islands are a subset of genomic islands that contain genes that contribute to the pathogenic potential of a specific strain. Pathogenicity islands are found to affect genomic diversity within a bacterial species in many bacteria. Extensive genetic rearrangements, and acquisition or loss of large blocks of DNA, may influence the evolution of non-pathogenic or less virulent strains into pathogenic variants.

I am interesting in the host-pathogen physiological and metabolic interactions. In this context, my work focuses in studying the host and pathogen metabolic adaptations in mouse burn models following P. aeruginosa acute or chronic infection. Aspects of the metabolism I am working on are oxidative stress mechanisms and energy production metabolic pathways.

Sepsis is a severe complication of burn that has become one of the major causes of death in burn patients. A thorough understanding of the epidemiology of sepsis in burns is thus a prerequisite in identifying and further investigating host and/or microorganism factors relevant to the high mortality of burn septic patients. Using the data collected from a large multi-center cohort study on Inflammation and Host Response to Injury (The Glue Grant), we will be searching for specific bio-markers of sepsis linked to poor outcome.

2000 Hasan Baydoun, American University of Beirut, Biological Sciences, Beirut Lebanon Summer Research

2003 Hasan Baydoun, American University of Beirut Medical Center, Beirut Lebanon