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Dr. Erle received an A.B. degree (Biochemistry) from Harvard College in 1980 and an M.D. degree from UCSF in 1984. He was trained in internal medicine and in pulmonary disease at UCSF. He joined the UCSF Lung Biology Center faculty in 1990. His academic activities include laboratory research and clinical teaching. He is the Director of the Functional Genomics Core Facility, UCSF Sandler Center for Basic Research in Asthma, Director of the UCSF NHLBI Shared Microarray Facility, and Associate Program Director for Genomics of the UCSF/SFGH General Clinical Research Center (GCRC). He is a member of the UCSF Program in Immunology and the Cardiovascular Research Institute. He serves as an Attending Physician in the San Francisco General Hospital Medical ICU and the Pulmonary Consultation Service.
Research Interests
The role of T cell cytokines in murine models of asthma. T helper cells are increased in airways of people with asthma. In animal models, cytokines produced by these cells cause airway inflammation, mucus overproduction, and airway hyperresponsiveness (all of which are hallmarks of asthma). We are now working with a variety of mouse models of asthma in order to understand the mechanisms of these cytokine effects. For example, we have produced transgenic mice that lack the capacity to respond to specific cytokines in all cells except airway epithelial cells. These experiments, together with experiments involving cultured human lung cells, allow us to directly determine how the effects of these cytokines on epithelial cells contribute to asthma pathogenesis.
Functional genomics. The sequencing of the human genome marks the beginning of a new era in biological research. We are producing tools that allow for the large-scale analysis of gene expression in human and mouse cells and tissues. The current focus is on the production and use of oligonucleotide microarrays. We are working closely with collaborators at UCSF and elsewhere, and are using microarrays to address problems relevant to asthma and other lung diseases.
Selected Recent Publications
Kuperman DA, Lewis CC, Woodruff PG, Rodriguez MW, Yang YH, Dolganov GM, Fahy JV, Erle DJ. Dissecting asthma using focused transgenic modeling and functional genomics. J Allergy Clin Immunol, 116:305-311, 2005. [Abstract]
Koth LL, Rodriguez MW, Berstein XL, Chan S, Huang X, Charo IF, Rollins BJ, Erle DJ. Aspergillus antigen induces robust Th2 cytokine production, inflammation, airway hyperreactivity and fibrosis in the absence of MCP-1 or CCR2. Respiratory Res 5:12, 2004. [Abstract] [Full text]
Kuperman D, Huang X, Koth LL, Chang GH, Dolganov GM, Zhu Z, Elias JA, Sheppard D, Erle DJ. Direct effects of interleukin-13 on epithelial cells cause airway hyperreactivity and mucus overproduction in asthma. Nature Med 8:885-9, 2002. [Abstract] [PDF]
Venkayya R, Lam M, Rodriguez M, Grünig G, Corry DB, Erle DJ. The Th2 lymphocyte products IL-4 and IL-13 rapidly induce airway hyperresponsiveness through direct effects on resident airway cells. Am Rev Respir Cell Mol Biol 26:202-8, 2002. [Abstract] [Full text]
Zhen G, Park SW, Nguyenvu LT, Rodriguez MW, Barbeau R, Paquet AC, Erle DJ. IL-13 and epidermal growth factor receptor have critical but distinct roles in
epithelial cell mucin production.
Am J Respir Cell Mol Biol. 2007 Feb;36(2):244-53.
Woodruff PG, Koth LL, Yang YH, Rodriguez MW, Favoreto S, Dolganov GM, Paquet
AC, Erle DJ.
A distinctive alveolar macrophage activation state induced by cigarette smoking.
Am J Respir Crit Care Med. 2005 Dec 1;172(11):1383-92.
Kuperman DA, Huang X, Nguyenvu L, Holscher C, Brombacher F, Erle DJ.
IL-4 receptor signaling in Clara cells is required for allergen-induced mucus
production.
J Immunol. 2005 Sep 15;175(6):3746-52.
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