Abstract

: Atherosclerosis is the principal contributor to the pathogenesis of myocardial and cerebral infarction, and no effective treatment is yet available for atherosclerosis. Identifying the etiological causes and understanding the pathogenic mechanisms of atherosclerosis may provide information for developing efficient strategies for preventing and/or controlling cardiovascular disease pathogenesis. Both epidemiological investigations and animal model studies have linked C. pneumoniae infection to atherosclerosis. The objectives of the present proposal are to further evaluate the role of C. pneumoniae infection in atherosclerosis in a mouse model system and to use this animal system to understand the mechanisms of C. pneumoniae atherogenesis by testing an infection / inflammatory response hypothesis. Specifically, the roles of both inflammatory responses and lipoprotein oxidation in C. pneumoniae exacerbation of atherosclerosis will be evaluated. These studies may provide the essential information on designing effective approaches for preventing and controlling C. pneumoniae-exacerbated atherosclerosis.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL064883-02
Application #
6537815
Study Section
Bacteriology and Mycology Subcommittee 2 (BM)
Program Officer
Rabadan-Diehl, Cristina
Project Start
2001-07-01
Project End
2005-06-30
Budget Start
2002-07-01
Budget End
2003-06-30
Support Year
2
Fiscal Year
2002
Total Cost
$252,875
Indirect Cost

  Institution

Name
University of Texas Health Science Center San Antonio
Department
Microbiology/Immun/Virology
Type
Other Domestic Higher Education
DUNS #
800772162
City
San Antonio
State
TX
Country
United States
Zip Code
78229

  Publications

Dong, Feng; Pirbhai, Mustak; Xiao, Yangming et al. (2005) Degradation of the proapoptotic proteins Bik, Puma, and Bim with Bcl-2 domain 3 homology in Chlamydia trachomatis-infected cells. Infect Immun 73:1861-4
Xiao, Yangming; Zhong, Youmin; Su, Heng et al. (2005) NF-kappa B activation is not required for Chlamydia trachomatis inhibition of host epithelial cell apoptosis. J Immunol 174:1701-8
Sharma, Jyotika; Niu, Yuhong; Ge, Jianbo et al. (2004) Heat-inactivated C. pneumoniae organisms are not atherogenic. Mol Cell Biochem 260:147-52
Dong, Feng; Sharma, Jyotika; Xiao, Yanming et al. (2004) Intramolecular dimerization is required for the chlamydia-secreted protease CPAF to degrade host transcriptional factors. Infect Immun 72:3869-75
Dong, Feng; Pirbhai, Mustak; Zhong, Youmin et al. (2004) Cleavage-dependent activation of a chlamydia-secreted protease. Mol Microbiol 52:1487-94
Greene, Whitney; Xiao, Yangming; Huang, Yanqing et al. (2004) Chlamydia-infected cells continue to undergo mitosis and resist induction of apoptosis. Infect Immun 72:451-60
Xiao, Yangming; Zhong, Youmin; Greene, Whitney et al. (2004) Chlamydia trachomatis infection inhibits both Bax and Bak activation induced by staurosporine. Infect Immun 72:5470-4
Sharma, Jyotika; Bosnic, Anthony M; Piper, Jeanna M et al. (2004) Human antibody responses to a Chlamydia-secreted protease factor. Infect Immun 72:7164-71
Su, Heng; McClarty, Grant; Dong, Feng et al. (2004) Activation of Raf/MEK/ERK/cPLA2 signaling pathway is essential for chlamydial acquisition of host glycerophospholipids. J Biol Chem 279:9409-16
Dong, Feng; Su, Heng; Huang, Yanqing et al. (2004) Cleavage of host keratin 8 by a Chlamydia-secreted protease. Infect Immun 72:3863-8

Showing the most recent 10 out of 12 publications