This Core will breed congenic mouse strains required for three of the four projects of the Center. Five knockout (null) mice strains and corresponding congenic wild-type mice and one conventional transgenic and corresponding wild-type congenic littermate will be bred and provided to the Project Leaders of individual projects for experimentation. The utilization of congenic mouse strains will circumvent the potential problem of confounding effects contributed by differences at genetic loci other than those being tested. For two of the null transgenic strains, mutant and wild-type congenic derivatives will be generated using the """"""""speed congenics"""""""" procedure which can generate congenic lines differing at less than 0.5 percent of the genome within five generations, rather than the ten required for the conventional congenic procedure. All congenics will be generated in the C57BL/6 mouse strain, which we have developed as a model for DEP-induced allergic hyperresponsiveness. Another service of the Core will be to genotype mice for the transgenic mutations. Two mouse strains, that are yet to be obtained from other collaborators, may be infected. If necessary, the Core will be responsible for rederiving these strains. In one project, mice will be exposed to TCDD, which is a potent carcinogen. The Core will be responsible for exposing the mice to TCDD in an acceptable and safe fashion, and for appropriate handling of contaminated material.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI050495-02
Application #
6663331
Study Section
Special Emphasis Panel (ZAI1)
Project Start
2002-09-01
Project End
2003-06-30
Budget Start
Budget End
Support Year
2
Fiscal Year
2002
Total Cost
Indirect Cost
Name
University of California Los Angeles
Department
Type
DUNS #
119132785
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
Riedl, Marc A; Saxon, Andrew; Diaz-Sanchez, David (2009) Oral sulforaphane increases Phase II antioxidant enzymes in the human upper airway. Clin Immunol 130:244-51
Schroder, Nicolas W J; Crother, Timothy R; Naiki, Yoshikazu et al. (2008) Innate immune responses during respiratory tract infection with a bacterial pathogen induce allergic airway sensitization. J Allergy Clin Immunol 122:595-602.e5
Xia, Tian; Kovochich, Michael; Nel, Andre E (2007) Impairment of mitochondrial function by particulate matter (PM) and their toxic components: implications for PM-induced cardiovascular and lung disease. Front Biosci 12:1238-46
Gilliland, Frank D; Li, Yu-Fen; Gong Jr, Henry et al. (2006) Glutathione s-transferases M1 and P1 prevent aggravation of allergic responses by secondhand smoke. Am J Respir Crit Care Med 174:1335-41
Nel, Andre; Xia, Tian; Madler, Lutz et al. (2006) Toxic potential of materials at the nanolevel. Science 311:622-7
Wan, Junxiang; Diaz-Sanchez, David (2006) Phase II enzymes induction blocks the enhanced IgE production in B cells by diesel exhaust particles. J Immunol 177:3477-83
Riedl, Marc A; Landaw, Elliot M; Saxon, Andrew et al. (2005) Initial high-dose nasal allergen exposure prevents allergic sensitization to a neoantigen. J Immunol 174:7440-5
Xiao, Gary Guishan; Nel, Andre E; Loo, Joseph A (2005) Nitrotyrosine-modified proteins and oxidative stress induced by diesel exhaust particles. Electrophoresis 26:280-92
Xia, Tian; Korge, Paavo; Weiss, James N et al. (2004) Quinones and aromatic chemical compounds in particulate matter induce mitochondrial dysfunction: implications for ultrafine particle toxicity. Environ Health Perspect 112:1347-58
Finkelman, Fred D; Yang, Mingyan; Orekhova, Tatyana et al. (2004) Diesel exhaust particles suppress in vivo IFN-gamma production by inhibiting cytokine effects on NK and NKT cells. J Immunol 172:3808-13

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