Antimicrobial resistance (AMR) poses a significant threat to human, animals and the environment. Dr. Jayachandran’s primary research interest is understanding the genetic basis of antibiotic resistance in methicillin-resistant Staphylococcus aureus (MRSA), a gram positive pathogen that causes nearly 11,000 deaths each year in the United States alone. Her research focuses on the role of SOS and stress (ROS, antibiotic) response in acquisition of antibiotic resistance in Staphylococcus aureus. Bacterial DNA damage stress response, also known as SOS response, includes a conserved set of genes that are induced under DNA damaging conditions. Among these are genes involved in DNA repair pathway and error-prone polymerases. The increased expression of error-prone polymerase result in increased rate of mutations, which contribute to antibiotic resistance. RecA and LexA are the main modulators of this SOS response. Two main projects in the lab are: 1) Studying the effect of RecA inhibitors on the emergence of antibiotic resistance; 2) Identifying genes that play a role in SOS and stress response using a transposon mutant library. These studies will help us understand the pathogenicity and the mechanism of antibiotic resistance in MRSA and provide insights for the development of new therapeutics.
Dr. LaRocca’s research interest lies primarily in the mechanisms of eukaryotic programmed cell death or PCD. This includes the processes of apoptosis, necroptosis, and the molecular switches that balance the two pathways. Dr. LaRocca is particularly interested in the role of glucose in driving PCD. He is actively investigating the mechanism of hyperglycemic cell death and its role in the exacerbation of ischemic brain injury (stroke). A second project in his lab is an NIH-funded grant aimed at improving understanding of a type of red blood cell death called necroptosis and exploring ways to influence this process. Results from this work could one day lead to improved treatments for patients suffering from bacterial blood infections and other blood related disorders.
The major focus of Dr. Mahdinia’s research is towards microbial fermentation of value-added products, especially biopharmaceuticals. As a professor of CBET (Center for Biopharmaceutical Education and Training), Dr. Mahdinia is part of the CBET team that aims to educate undergraduate and graduate students and provide workforce training in the manufacturing of biopharmaceuticals. Thus, with all brand-new and cutting-edge equipment at CBET for upstream and downstream bioprocessing, virtually any novel research ideas in the field of fermentation products are welcome and feasible to carry out! For more information on CBET facilities and Dr. Mahdinia’s role at CEBT; check out the center’s facilities.
The long term research goal of Dr. Malik’s laboratory is to understand the complexities of host pathogen interactions for the development of improved prophylactics and therapeutics against important bacterial infections. She has a three-year grant by the National Institutes of Health to investigate the mechanisms by which Francisella tularensis, a category A biothreat agent survives inside the immune cells and suppresses the protective immune responses. A second area of focus is investigating the molecular mechanisms leading to the development of antibiotic resistance in methicillin resistant Staphylococcus aureus (MRSA) strains. Click the following PubMed link for additional information on research projects taking place in Dr. Malik's lab.
Dr. Parent is a trained microbiologist, clinical microbiologist, and immunologist. Her research is centered on understanding the immune response to infection, with a specific focus on two bacterial pathogens - Vibrio parahaemolyticus and Yersinia pestis. V. parahaemolyticus is a Gram-negative bacterium most commonly associated with the ingestion of raw oysters. Dr. Parent's research on this bacterium seeks to characterize which type of host response to infection may allow it to evade the host innate responses. Y. pestis is a facultative intracellular gram-negative bacillus. With this pathogen, the focus of the lab's work is to identify and understand those aspects of the immune response needed to survive a lethal pneumonic infection in order to produce a more efficacious vaccine.
Dr. Shakerley’s research interests include the study of Acinetobacter baumannii bacterium, a gram negative opportunistic pathogen that presents not only a nosocomial threat, but specifically impacts military personnel deployed to overseas theatres of operation. Currently, multidrug-resistant Acinetobacter species account for more than 7,000 infections in the United States per year which may be exacerbated by the pathogen’s innate ability to evade host immune defenses. One of the major areas of focus for her lab is the development of novel therapeutic strategies to combat antibiotic resistant nature of this pathogen.
For the vast majority of virus-types found on Earth, human cells are successful at defending themselves from invasion. However, many viruses that are significant human pathogens have evolved mechanisms to counter cellular defenses and thus enable disease spread. The majority of Dr. Sharifi’s research is focused on this evolutionary “arms race” between viruses and host-cells which has included deeper exploration of the HIV virus. This work has also helped lead to a better understanding of normal cell biology, which has subsequently opened doors to new questions and opportunities for student-centered research.
Dr. Shi’s research interests are mainly focused on understanding the molecular basis of disease pathogenesis by using advanced molecular biology, virology, molecular genetics, and bioinformatics approaches. Methods used in his lab include a) HIV-1 infectious molecular clone, recombinant virus, and reporter gene technologies to study HIV phenotypes such as infection and replication; b) HIV-1 single genome amplification, sequencing and bioinformatics tools to understand genotype changes and their association with disease progression. Another major area of interest in Dr. Shi’s lab is the design and development of diagnosis assays for detecting infectious diseases, monitoring disease progression, and managing treatments.
Dr. Singh has an extensive scientific background in studying molecular mechanisms associated with HIV pathogenesis, genomic imprinting, molecular biology and mouse models of disease. Dr. Singh’s research interests include investigating the underlying molecular mechanisms involved in- i) HIV associated neurological disorder, ii) HIV latency, and iii) Viral infection induced developmental defects. Currently, Dr. Singh’s lab is focused at investigating two projects that come under NIH HIV/AIDS high priority research topics. Project 1: To investigate the consequences of HIV (Human Immunodeficiency Virus) mediated downregulation of Sonic hedgehog (Shh) signaling on brain homeostasis with specific focus on aberrant communication between astrocytes and other brain-resident cells (brain endothelial cells, pericytes, microglia and neurons). Project 2: To characterize select noncoding RNAs for their potential to establish HIV latency via- i) mediating Interferon signaling, and ii) regulating expression of HIV genome by epigenetic mechanisms. Successful completion of these studies will identify novel targets to alleviate HIV pathogenesis as well as pave the way towards HIV cure.
Research in Dr. Yager’s laboratory is focused on understanding how the body regulates inflammatory responses during flu infection. Recent studies have established a critical role for the multi-protein cytosolic NLPR3 inflammasome complex in host defense and pathophysiology during flu infection. Specifically, Dr. Yager and his team are investigating how NLRP3 inflammasome activation and resultant inflammatory cytokine secretion are regulated on a molecular level to favor host protection over immunopathology. Other areas of research include the identification of novel targets for the development of new anti-viral drugs to combat flu infection and the role of viral-induced inflammation in the etiology and pathogenesis of autism spectrum disorder.