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BARRETT, EDWARD G., PHD CONTACT INFORMATION Fax: (505) 348-8567 e-mail: tbarrett@LRRI.org Extended CV

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EDUCATION
B.S. (Aerospace/Bioengineering) 1991, University of Colorado
M.S. (Aerospace/Bioengineering) 1993, University of Colorado
Ph.D. (Toxicology) 1999, University of Rochester

EMPLOYMENT

2007 - Present	Staff Scientist, Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, NM
2002 - 2007	Associate Staff Scientist, Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, NM
2001 - Present	Clinical Assistant Professor, College of Pharmacy, University of New Mexico, Albuquerque, NM
2000 - 2002	Associate Research Scientist, Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, NM
1999 - 2000	Postdoctoral Fellow, Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, NM
1991 - 1993	Graduate Research Assistant, Department of Aerospace Engineering, Center for Space Environmental Health, University of Colorado
1991 - 1992	Summer Engineering Intern, Marting Marietta Astronautics Group, Denver, CO
1989 - 1991	Undergraduate Research Assistant, Department of Aerospace Engineering, Center for Space Environmental Health, University of Colorado
Summer 1989	Hardware Inspector/Engineering Assistant, Storage Technology Corporation, Louisville, CO

AREAS OF RESEARCH
The major goal of Dr. Barrett's research is to understand the underlying cellular and molecular mechanisms which mediate the genetic and environmental factors that contribute to the development and exacerbation of asthma. Additionally, his lab is focused on utilizing different animal models of allergy/asthma to test and develop new drugs/therapies for the treatment of allergies/asthma. Three areas of research that are directed toward these goals include the contribution of ultrafine particles (air pollutants) in the development and exacerbation of asthma, maternal influence in asthma, and development of an asthma vaccine.

• Effects of Inhaled Ultrafine Particles on Asthma
  Epidemiological studies show that hospital admissions for asthma are positively associated with the concentrations of particulate matter (PM) in the air. However, experimental data are limited to support or contradict the possibility that the inhalation of low concentrations of ultrafine PM increases asthma attacks. Immune and inflammatory cells localized to the lungs of asthmatics respond to inhaled allergens with the production and release of inflammatory mediators that play central roles in asthma attacks. Although the inhalation of allergens usually stimulates the release of these inflammatory mediators, exposure to ultrafine particles may also trigger their release in the lungs of allergic individuals. We are currently performing studies to address two hypotheses: inhaled ultrafine particles trigger asthma attacks 1) directly by stimulating the release of allergic response mediators in the lungs of asthmatics, or 2) indirectly by decreasing the concentration of inhaled allergen necessary to cause asthma attacks.

• Maternal Influence in Asthma
  Genetic predisposition for the development of atopy and exposure to high levels of allergen during early childhood have been implicated as the major determining factors for the development of allergic disease. However, increasing evidence suggests that the mother plays an important role in influencing development of fetal and infant immune responses to allergen during gestation. We are testing the hypothesis that elevated levels of maternal antibodies specific for allergen during pregnancy are a risk factor for the development of childhood asthma. In addition, we are testing the hypothesis that exposure of an allergic mother to allergen during pregnancy will predispose the fetus to develop an allergic response to allergen following birth. We are currently defining a murine and canine model to directly test these hypotheses. If, as we hypothesize, the maternal environment is critical in the development of childhood asthma, further studies will examine which maternal/placental/fetal cells are important in mediating the development of the fetal immune response. Ultimately, understanding the maternal component of the risk for developing childhood asthma could lead to new treatment and prevention strategies.

• Asthma Vaccine
  Allergic asthma is characterized by a Th2 mediated immune response to allergen. Several lines of evidence suggest that Th1 (instead of Th2) like infections during childhood may be protective against the development of allergic disease. A novel approach to preventing allergic disease is to induce a Th1 immune response thereby preventing a Th2 response. Oligonucleotides containing CpG motifs are highly effective Th1-like vaccine adjuvants and have been successfully used to prevent the sensitization of mice to a Th2 allergen. We are in the process of characterizing the efficacy of various formulations of a ragweed-CpG conjugate to prevent or reverse allergic asthma in a canine model of asthma.

REPRESENTATIVE PUBLICATIONS

1. Barrett, E. G. K. Rudolph, L. E. Bowen and D. E. Bice: Parental Allergic Status Influences the Risk of Developing Allergic Sensitization and an Asthmatic-Like Phenotype in Canine Offspring. Immunology 110: 493-500, 2003.

2. Barrett, E. G., K. Rudolph, L. E. Bowen, B. A. Muggenburg and D. E. Bice: Effect of Inhaled Ultrafine Carbon Particles on the Allergic Airway Response in Ragweed Sensitized Dogs. Inhal. Toxicol. 15: 151-165, 2003.

3. Singh, S. P., E. G. Barrett, R. Kalra, S. Razani-Boroujerdi, R. J. Langley, V. Kurup, Y. Tesfaigzi and M. Sopori: Prenatal Cigarette Smoke Decreases Lung cAMP and Increases Airway Hyperresponsiveness. Am. J. Respir. Crit. Care Med. 168: 342-347, 2003.

4. Barrett, E. G., R. D. Henson, S. K. Seilkop, J. D. McDonald and M. D. Reed: Effects of Hardwood Smoke Exposure on Allergic Airway Inflammation in Mice. Inhal. Toxicol. 18(1): 33-43, 2006.

5. Head E., E. G. Barrett, M. P. Murphy, P. Das, M. Nistor, F. Sarsoza, C. C. Glabe, R. Kayed, S. Milton, V. Vasilevko, N. W. Milgram, M. G. Agadjanyan, D. H. Cribbs, and C. W. Cotman: Immunization with Fibrillar Ab_1–42 in Young and Aged Canines: Antibody Generation and Characteristics, and Effects on CSF and Brain Ab. Vaccine 24(15): 2824-2834, 2006.

6. Phaybouth, V., S. Z. Wang, J. A. Hutt, J. D. McDonald, K. S. Harrod and E. G. Barrett: Cigarette Smoke Suppresses Th1 Cytokine Production and Increases RSV Expression in a Neonatal Model. Am. J. Physiol. Lung Cell. Mol. Physiol. 290(2): L222-L231, 2006.

7. McDonald, J. D., M. D. Reed, M. J. Campen, E. G. Barrett, J. Seagrave and J. L. Mauderly: Health Effects of Inhaled Gasoline Engine Emissions. Inhal. Toxicol. 19(Suppl. 1): 107-116, 2007.

8. Barrett, E. G.: Maternal Influence in the Transmission of Asthma Susceptibility. Pulm. Pharmacol. Ther. 21(3): 474-484, 2008.

9. Day, K. C., M. D. Reed, J. D. McDonald, S. K. Seilkop and E. G. Barrett: Effects of Gasoline Engine Emissions on Preexisting Allergic Airway Responses in Mice. Inhal. Toxicol. 20(13): 1145-1155, 2008.

10. Head, E., V. Pop, V. Vasilevko, M. Hill, T. Saing, F. Sarsoza, M. Nistor, L. A. Christie, S. Milton, C. Glabe, E. Barrett and D. Cribbs: A Two-Year Study with Fibrillar b-Amyloid (Ab) Immunization in Aged Canines: Effects on Cognitive Function and Brain Ab. J. Neurosci. 28(14): 3555-3566, 2008.

11. Reed, M. D., E. G. Barrett, M. J. Campen, K. K. Divine, A. P. Gigliotti, J. D. McDonald, JC. Seagrave, J. L. Mauderly, S. K. Seilkop and J. A. Swenberg: Health Effects of Subchronic Inhalation Exposure to Gasoline Engine Exhaust. Inhal. Toxicol. 20(13): 1125-1143, 2008.

12. Xu, J., F. Xu and E. Barrett: Metalloelastase in Lungs and Alveolar Macrophages is Modulated by Extracellular Substance P in Mice. Am. J. Physiol. Lung Cell. Mol. Physiol. 295(1): L162-L170, 2008.