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John Steinke

Steinke, John

Primary Appointment

Associate Professor, Medicine

Education

  • PhD, Allergy & Immunology, Texas A&M University

Contact Information

PO Box 801355
MR-4, Rm. 5041
Telephone: 434-982-3270
Fax: 434-924-5779
Email: js3ch@virginia.edu

Research Interests

Phenotypic analysis of chronic rhinosinusitis, epithelial immune response to rhinovirus infection, functional characterization of the IL-5 receptor in severe asthma and functional analysis of genes involved in asthma and sinus disease.

Research Description

1) Molecular genetic studies in allergic disease and asthma:

Polymorphisms have been described in the interleukin (IL)-10 and transforming growth factor IL-9 promoters that link in several population studies to the presence of allergies and asthma. The IL-10 promoter polymorphism is a C/A base exchange at 517 that is located between putative binding sites for two transcription factors. We are currently looking at the role of the IL-8 polymorphism in predicting which patients have severe allergic reactions following rhinovirus infection.

2) Determine the molecular mechanism of nasal polyp formation:

Nasal polyposis is a disease characterized by the recurrent growth of tissue from the middle turbinant of the sinus tissue. The mechanism of polyp formation is unknown so we are characterizing the cellular components that are involved in directing and maintaining polyp growth. We have found and overexpression of cysteinyl leukotrienes and the enzymes involved in their synthesis is polyp tissue sub-types compared to controls. Additional work is centered on determining the role that hypoxia plays in promoting the fibrosis observed in non-eosinophilic sinusitis.

3) Innate and adaptive responses to rhinovirus infection:

The epithelium is the primary site of rhinovirus (RV) infection. We are investigating the inflammatory response generated following RV infection with interest in the asthmatic cohort as this group has been shown to be susceptible to exacerbations induced following infection with RV. In particular, we are identifying the signaling pathways that lead to production of Th2 cytokines responsible for induction of the Th2 T cell response found in asthma. A second arm of our studies is involved in the CD8 T cell response to RV and the deviation to a Tc2 cytokine profile expressed by these cells.

Selected Publications