Postdoctoral Associates 

Sara Jones

Dr. Sara Jones

Ph.D., Baylor College of Medicine, Houston, TX 2008

Beneficial microbes limit disease caused by invading pathogens; however, the mechanisms and genes utilized by beneficial microbes to inhibit pathogenesis are poorly understood. Bacillus subtilis is a spore-forming bacterium present in the gut of mammals and B. subtilis spores have been used to prevent intestinal disease. B. subtilis limits intestinal disease induced by the murine pathogen Citrobacter rodentium, which is genetically similar to the human pathogens enterohemorrhagic and enteropathogenic E. coli. I want to determine the B. subtilis genes required for protection and elucidate the host pathways modulated by B. subtilis. By expanding our current mechanistic knowledge of bacterial protection, we could better utilize beneficial microbes to prevent intestinal disease caused by pathogenic bacteria.

Dr. Jung Eun Park

Dr. Jung-Eun Park

Ph.D.,Chungnam National University, Daejeon, Korea, 2012

Cells recognize virus infection and develop rapid and potent antiviral responses. Interferon (IFN) is well-known innate immune responses and induces the transcription of hundreds of different IFN-stimulated genes (ISGs) to control virus invasion. These ISGs encode distinct proteins with diverse biological effects that block multiple stages of the viral replication cycle, including entry into host cells, protein translation, replication, assembly of new virus particles and spread. IFN-Induced Trans-Membrane (IFITM) proteins are the only known ISGs that block viruses at the cell entry stage. While the underlying mechanisms of this antiviral activity are not fully determined, current evidences suggests that IFITM proteins block virus-cell membrane fusions. My research goal is to evaluate the mechanism of IFITM3-mediated virus entry restriction in relation to host proteins, to determine how IFITM3 operates in conjunction with other host cell proteins. For the study, I employed coronaviruses; enveloped RNA viruses that can enter cells by fusion with endosomal membranes or with plasma membranes depend on the presence of proteases. This study will provide critical information to understand the mechanisms of action of IFITM3 proteins and how cells interfere virus entry.

Dr. Doerte Lehmann

Dr. Doerte Lehmann

Ph.D., University of Rostock, Rostock, Germany, 2012

Dr. Julie Swartzendruber

Dr. Julie Swartzendruber

Ph.D., Northwestern University, Evanston, IL, 2013

Yougang Zhai

Dr. Yougang Zhai

Ph.D., Institute for Viral Disease Control and Prevention, China CDC, China, 2008

Because mucosal tissue is one of the major sites of HIV infection, an effective HIV vaccine must induce both systemic and mucosal immunity to contain virus transmission through hematogenous or sexual pathway. Mucosal immunization can induce both mucosal and systemic immunity, including neutralizing antibodies and cytotoxic T lymphocytes. In Dr. Qiao's Lab, we are trying to develop mucosa vaccines to prevent HIV-1 infection. The overall goal of my study is to develop effective mucosa vaccine(s) for HIV-1. Two approaches will be applied for the vaccine design. Briefly, we will develop chimeric virus-like particles (CVLPs) containing conserved epitopes that can be recognized by HIV-1 broadly neutralizing antibodies. On the other hand, we will also develop pseudovirus vaccine that is comprised of empty viral capsid and foreign plasmid DNA. Eventually, HIV-1 specific immune response(s) induced by either vaccine will be determined. This work will benefit the development of a novel effective mucosal vaccine for HIV-1.

Ekaterina Semenyuk

Dr. Ekaterina Semenyuk

Ph.D., Plant Physiology, Timiryazev Institute of Plant Physiology, Moscow, Russia, 2003

Clostridium difficile infection is a devastating gastrointestinal disease and a major problem in hospitals world wide. Complicating treatment is the capacity of the disease to persist in the host after apparently successful antibiotic treatment.
Our central hypothesis is that C. difficile forms abiofilm in the host gastrointestinal tract. C. difficile biofilms could contribute to disease by 1) facilitating attachment of C. difficile to appropriate locations in the colon, 2) resisting host defenses and antimicrobial drugs, 3) accumulating toxin and directing it to host tissues, and 4) by harboring a depot of dormant spores that could facilitate relapsing disease. Understanding C. difficile biofilm structure and mechanisms used by this organism to evade host defenses and therapeutics would greatly facilitate development of novel treatments.

Xufang Deng

Dr. Xufang Deng

Ph.D., Shanghai Veterinary Research Institute, CAAS, China, 2011

Coronaviruses cause important human and animal disease with respiratory, gastrointestinal and neurological symptoms. The severe acute respiratory syndrome coronavirus (SARS-CoV) emerged from Guangdong province of China in 2003, which infected more than 8000 people worldwide with 10% mortality, promotes to investigate the viral pathogenesis and to develop antiviral agents. In previous studies of Dr. Baker’ Lab, the Papain-like proteases (PLPs) of coronaviruses have been identified to possess deubiquitinating enzyme, deISGylating enzyme activities and act as IFN antagonism. My research mainly focuses on further elucidating the mechanism of PLpro-mediated evasion of innate immune response. We will determinate the effect of PLPs to disturb the ubiquitination and ISGylation of cellular proteins in mice infected with recombinant Sindbis virus co-expressing ISG15 and PLPs (rSinV-ISG15-PLPs). And we will evaluate the immune response of mice infected by rSinV-ISG15-PLPs or PLPs mutants. This work will further demonstrate the biological functions of PLPs and highlight its significance as a target of developing antiviral drugs.

Dr. Tyler Boone

Dr. Tyler Boone

Ph.D., University of Alberta, Edmonton, Alberta, Canada, 2012

Bacillus anthracis remains a biological threat, both as a potential weapon and as a natural pathogen in areas where it is endemic. The overall goal to my research is to develop a novel vaccine targeting the B. anthracis spore, which could be used to prevent disease caused by B. anthracis. To date, I have produced and purified a number of spore surface proteins as well as one subunit of the toxin, which have been assayed in a mouse model for their ability to induce an immune response. Since it is possible to modify the outer surface of the B. anthracis spore, through mechanical and genetic methods, without affecting virulence it is necessary to identify antigens that would be surface expressed under these conditions. In addition to producing spore surface proteins, my research involves generating mutations that affect spore surface antigens, assessing the effect these mutations may have on virulence, and identifying alternative surface proteins to target these mutant strains.  

Mariko Takami

Dr. Mariko Takami

Ph.D., Loyola University Chicago, Chicago, IL, 2012

CD4+ T cells play a major role in orchestrating other immunecells by producing cytokines and chemokines; hence, they are referred to ashelper T cells. The helper T cells are classified into smaller subsetsdepending on which cytokines they produce. Th9 cells are aCD4+ helper T cell subset that produces IL-9, a pleiotropic cytokine that regulatesa variety of immune cells including T cells, B cells and mast cells. Recentstudies demonstrated that Th9 cells inhibit tumor growth in a mast celldependent manner using a mouse in vivo model. The data indicate that Th9 cells play an important role in anti-tumorimmunity. It is well established that mouse na´ve CD4 T cells differentiateinto Th9 cells when stimulated by antigen in the presence of TGF-b and IL-4. However, how human na´ve CD4+Tcells differentiate into Th9 cells is not well understood. My research goal isto determine the mechanism by which human Th9 cells are induced. This willprovide a potential method for human Th9 induction and expansion and can beapplicable for anti-tumor immune therapy.

Dr. Ute Osmers

Dr. Ute Osmers

Ph.D. Loyola University Chicago, Chicago, IL, 2003

The rabbit is an excellent model for studying the decline ofB lymphopoiesis with age. The long bones of rabbits fill up with adipocytes startingat 2 months of age, resembling the bone marrow of humans over the age of 60. Workin our lab has shown that factors secreted by adipocytes arrest B celllymphopoiesis beyond the pre B cell stage. The identification of the factorsand their mechanisms is an ongoing process in our lab.

Adipocytes, osteoblasts and chondrocytes arise from a commonprecursor, the mesenchymal stromal cell, also called mesenchymal stem cell(MSC). We are characterizing MSCs isolated from rabbits of various ages toassess which mechanisms within the cells lead to preferred differentiation intoadipocytes to the expense of osteoblasts. We propose that an underlyingepigenetic shift occurs with age or hormonal maturity leading to theaccumulation of adipocytes and decline of B cell lymphopoiesis.



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