Giulio Taglialatela, Ph.D.
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The role of environmental toxicants, such as gaseous and particulate air pollutants, in promoting airway inflammation and hyperresponsiveness may be important in the development of asthma and chronic obstructive pulmonary disease. Our studies include the role of sulfur dioxide (SO2) in animal models and human cell cultures, with focus on the production of reactive oxygen species and subsequent intracellular signaling as the driving force behind the development of airway inflammation in response to environmental pollutants. An important cytokine in the inflammation resolution may be IL-10, which is known to be inhibited in asthma, and may be a reason for the sensitivity of asthmatics to SO2, as compared to non-asthmatics. Utilization of IL-10 knockout mice models this situation, allowing testing of this hypothesis and investigation of its origins. Also of interest are the effects of carbon monoxide (CO) on airway inflammation, potentially through this same cytokine effect node, and its association with nitric oxide (NO) produced within the airway.
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William J Calhoun MD has several principal themes in his laboratory, all of which relate to the role of inflammation and its control in asthma and other airway diseases. First, we are interested in cytokine control of allergic inflammation in asthma. We have made original observations on the role of interleukin-10 as a controller of allergic inflammation. This line of work interfaces with the animal models Dr Ameredes has developed. Secondly, we have novel tools for measuring the function of glucocorticoid receptors [GR]. The regulation of GR by inflammatory cytokines, allergic mediators, oxidants, and anti-inflammatory drugs is a central focus of the laboratory. We have shown that soluble factors from the airway of asthma subjects block GR signaling. Finally, we are also interested in the discovery of biomarkers of asthma severity, and response to therapy in asthma. Using state-of-the-art proteomics in collaboration with Drs Alex Kurosky and John Wiktorowicz, and advanced bioinformatics and biostatistics with Drs Allan Brasier and Suresh Bhavnani, we are searching for predictive biomarkers that distinguish severe asthma from milder forms of the disease, and for biomarkers that predict the response to treatment with steroids or other control medications. Because we are part of two national networks for asthma, we have access to a broad range of clinical samples.
4. The Cheng laboratory has been using multidisciplinary approaches, coupling biochemistry and biophysics with cell biology and pharmacology, to understand the structure and function of exchange protein directly activated by cAMP (Epac) and oncogene KRAS. Our long-term goals are to unravel the signaling intricacies of Epac and KRAS and to design pathway specific inhibitors for these important signaling molecules so that their functions can be pharmaceutically exploited and modulated for the treatment of human diseases.
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