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C.S. Mott Children's Hospital

Research

lipuma

JOHN J. LIPUMA, MD
James L. Wilson, M.D., Research Professor of Pediatrics and Communicable Diseases
Professor of Epidemiology, School of Public Health
Division Director, Pediatric Infectious Diseases

(jlipuma@umich.edu)

Research Program

Dr. LiPuma directs the Cystic Fibrosis Foundation Burkholderia cepacia Research Laboratory and Repository at the University of Michigan. Research in this laboratory focuses on infectious diseases in persons with cystic fibrosis, with an emphasis on the epidemiology, ecology, natural history, clinical microbiology, taxonomy and pathogenicity of bacteria in the Burkholderia cepacia complex.

Current studies include analyses of the population genetic structure and evolution of B. cepacia complex; the natural history of infection by B. cepacia complex and related bacterial species in cystic fibrosis; virulence factors and pathogenic mechanisms of B. cepacia complex: and molecular epidemiology of B. cepacia complex and related species.
Research Lab: 734-936-9767

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R. ALEXANDER BLACKWOOD, MD, PHD
Associate Professor of Pediatrics
(rab@umich.edu)

Research Program: Innate Host Defense Research

Research in this laboratory is focused on the human cellular response to bacterial invasion, specifically, the mechanism of neutrophil degranulation. The primary goal is to identify and characterize the signaling and biochemical events mediating the actual fusion of neutrophil granules with the forming phagosome. We have developed both cellular and cell free assays to model the neutrophil secretory system evaluating the interplay between fluxes in intracellular calcium concentration, changes in membrane phospholipid composition, protein kinase activation and cytosolic and membrane proteins. Recent investigations have focused on examining the role of lipid compartments (rafts) in granule plasma membrane fusion.

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dawid

SUZANNE R. DAWID, MD, PHD
Assistant Professor of Pediatrics
(sdawid@med.umich.edu )

Research Program

Disease caused by the bacteria Streptococcus pneumoniae (pneumococcus) varies from relatively benign middle ear infections and sinusitis to life threatening meningitis and pneumonia. Pneumococcal infections, which primarily affect children under two and adults over 65 years of age, kill approximately 1 million children each year world wide, with the greatest impact in the developing world. Despite the severity of some infections with pneumococcus, the majority of young children carry the organism in their noses asymptomatically. Since the introduction of the seven-valent pneumococcal vaccine in the United States eight years ago, the incidence of severe pneumococcal disease has dropped dramatically. This vaccine targets the seven “types” (out of over 90 types known) most often associated with invasive disease in the United States. Despite the dramatic decline in infections as a result of vaccination, new, previously rare types have begun to replace the targeted organisms. More worrisome is that some of these replacement types are resistant to many of the antibiotics routinely used for treatment.

We do not understand what factors allow one type of pneumococcus to out-compete another type. My laboratory is interested in determining what allows this bacterial pathogen to survive and compete in the human nose. Because nasal colonization is the first step in pneumococcal disease, understanding what factors are required for success in this environment will allow us to better predict the outcome of vaccination. In addition, we hope to use the strategies that have been refined by bacterial competitors over millions of years to discover new approaches

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gilsdorfJANET R. GILSDORF, MD
Robert P. Kelch Research Professor of Pediatrics
Professor of Epidemiology, School of Public Health

gilsdorf@med.umich.edu

Research Program:


The Haemophilus influenzae Research Laboratory, funded by the National Institutes of Health, studies the interactions between bacteria and humans during H. influenzae colonization and infection. The goal of these studies is to identify strategies to prevent sinusitis, otitis media, and bronchitis caused by H. influenzae.

Current ongoing studies include a molecular and evolutionary analysis of H. influenzae virulence factors associated with asymptomatic colonization, acute otitis media, chronic obstructive pulmonary disease (COPD) and bacterial transmission; molecular mechanisms of H. influenzae antigenic diversity; and molecular epidemiology of H. influenzae colonization and infection.

Laboratory Investigators:
Janet R. Gilsdorf, MD, Robert P. Kelch Research Professor of Pediatrics
Carl Marrs, PhD, Associate Professor of Epidemiology
Lixin Zhang, PhD, Research Assistant Professor of Epidemiology
May Patel, MS, Research Associate

Collaborators:
The Center for Molecular and Clinical Epidemiology of Infectious Diseases is a multi-discipline center promoting laboratory and field studies related to infectious diseases.

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dr. terri stillwellTERRI L. STILLWELL, MD, MPH
Clinical Assistant Professor of Pediatrics
(tstillwe@med.umich.edu)

Research Program:

Clinical research in hospital epidemiology and bacterial resistance as it relates to nosocomial infections and antimicrobial stewardship.

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JASON B. WEINBERG, MD
Associate Professor of Pediatrics
Associate Professor of
Microbiology and Immunology
(jbwein@umich.edu)

Research Program: Pathogenesis of Adenovirus Respiratory Infections

The human adenoviruses cause a wide range of clinical disease, ranging from mild upper respiratory tract infections in otherwise normal individuals to overwhelming disseminated infection and death in immunocompromised patients.  Persistent adenovirus infections have been linked to chronic lung diseases such as asthma and chronic obstructive pulmonary disease.  Much of our laboratory’s research is focused on adenovirus pathogenesis, defining interactions between adenoviruses and host inflammatory responses.  We use a mouse adenovirus to study issues of viral persistence, host immune responses to infection, and interactions between the two processes.  We are interested in the ability of a persistent adenovirus to modulate host immunologic and physiologic responses induced by subsequent stimuli.  In addition, we hope to define ways in which aberrant host inflammatory responses, such as exaggerated T-helper type 2 cytokine production in asthma or eicosanoid overproduction in bone marrow transplantation, may influence viral replication and alter host susceptibility to viral infection. 

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