Hydar Ali, Ph.D. Associate Professor Contact Information Robert Schattner Center University of Pennsylvania School of Dental Medicine Rm 346 Levy Building 240 South 40th Street Philadelphia, PA 19104-6030 Phone 215-573-1993 Email: ali@path.dental.upenn.edu

Training:

• Research Associate, National Institutes of Health, Bethesda, MD., 1989-1991
• Postdoctoral Fellow, National Institutes of Health, Bethesda, MD., 1986-1989
• Ph.D. University College London, England., 1982-1986

Research Interests:
Despite improved living conditions, widespread vaccination and the availability of antibiotics, infectious diseases continue to take a heavy toll in the United States. In developing countries, it is estimated that infectious diseases kill more than 10 million people each year. The predominant cell type that functions as a sentinel to limit microbial infection is the mast cell. Mast cells are found at sites that are exposed to the external environment, such as the skin, the airway and the intestine and are armed with receptors (Toll-like receptors; TLRs) that directly interact with bacteria and other pathogens, resulting in the release of chemical mediators. These mast cell-derived mediators recruit neutrophils at the site of infection, which eliminate the infectious agents. One component of our research is to delineate the molecular mechanism by which bacterial pathogens activate mast cells and to understand how TLR functions are regulated.

Mast cells not only mediate innate immunity but also play central roles in a variety of inflammatory diseases. Another focus of our research is to understand the role of G protein coupled receptor signaling in the pathogenesis of allergic asthma. More specifically, we are interested in delineating the signaling pathway via which complement component C3a promotes mast cell degranulation and NF-kappa activation and to understand the molecular mechanisms via which functions of G protein coupled receptor functions are regulated in mast cells.

Selected Publications:

• Venkatesha, R. T., Ahamed, J., Nuesch, C., Zaidi, A. K and Ali, H. Platelet-activating factor-induced chemokine gene expression requires NF- k B activation and Ca2+/calcinuerin signaling pathways: Inhibition by receptor phosphorylation and b -arrestin recruitment. J. Biol. Chem. 279, 44606-44612, 2004.
• Venkatesha, R. T., Thangam, E. B., Zaidi, A. K.and Ali, H. Distinct regulation of C3a-induced MCP-1/CCL2 and RANTES/CCL5 production in human mast cells by extracellular signal regulated kinase and PI3 kinase. Mol. Immunol. 42, 581-587, 2005.
• Thangam, E. B., Venkatesha, R. T., Zaidi, A. K., Jordan-Sciutto, K. L., Goncharov, D. A., Krymskaya, V. P., Amrani, Y., Panettieri R. A., and Ali, H. Airway smooth muscle cells enhance C3a-induced mast cell degranulation following cell-cell contact. FASEB J. 19, 798-800, 2005.
• Ali, H. and Panettieri, R. A. Anaphylatoxin C3a receptors in asthma. Respiratory Research 6:19, 2005.
• Thangam, E. B., Venkatesha, R. T., Zaidi, A. K., Jordan-Sciutto, K. L., Goncharov, D. A., Krymskaya, V. P., Amrani, Y., Panettieri R. A., and Ali, H. Airway smooth muscle cells enhance C3a-induced mast cell degranulation following cell-cell contact. FASEB J . 19, 798-800, 2005.
• Ali, H. and Panettieri, R. A. Anaphylatoxin C3a receptors in asthma. Respiratory Research. 6: 19, 2005.
• Zaidi, A. K., Amrani, Y., Panettieri R. A., and Ali, H. Response to C3a, mast cells, and asthma. FASEB J. 20, 199, 2006.
• Ali, H and Haribabu, B. (Editors). Transmembrane Signaling Protocols. Methods in Molecular Biology, Human Press. 332, 2006.
• Zaidi, Thangam, E.B., Ali, H. Distinct regulation of Toll-like receptor function in a human mast cell line (LAD2) and murine Lung mast cells: Role of G protein and Ca2+ mobilization Immunology (in press) 2006.
• Zaidi, A. K and Ali, H: C3a receptor signaling in mast cells. Advances in Experimental Medicine and Biology Series, editor John D. Lambris (Springer) (in press).

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