Chlamydia trachomatis is an obligate intracellular bacterial pathogen and a leading cause of sexually transmitted bacterial diseases. C. trachomatis organisms have adapted an intravacuolar replication life cycle and can persist in the infected hosts for a long period of time. The chlamydial persistence, a major cause of chlamydia-induced diseases in humans, may be due to chlamydial ability to evade host immune responses. T cell-mediated immunity plays important roles in controlling intracellular infections. Chlamydia has evolved various strategies for evading host defense, including inhibition of phagolysosomal fusion, alteration of host cell signaling pathways and inhibition of MHC antigen presentation. Research work from Dr. Zhong's lab is focused on understanding how chlamydia evades host immune mechanisms. After correlating the chlamydial suppression of MHC antigen expression with chlamydial degradation of host transcription factors, Dr. Zhong's lab has identified a chlamydia-secreted protein designated as CPAF (chlamydia-specific protease/proteasome-like activity factor) that is responsible for the chlamydial degradation of host transcription factors required for MHC gene activation. Interestingly, CPAF is synthesized as a 70kDa proprotein and rapidly processed into a 29 kDa N-terminal (CPAFn) and a 35kDa C-terminal (CPAFc) fragments. The CPAFn and c fragments form functional and stable intramolecular dimers. Dr. Zhong's lab will continue to understand the mechanisms of CPAF activation and activity using various biochemical, immunological, molecular and cellular approaches. These studies will provide important knowledge for developing strategies to prevent/block chlamydial immune evasion. ? ?

National Institute of Health (NIH)
National Institute of Allergy and Infectious Diseases (NIAID)
Research Project (R01)
Project #
Application #
Study Section
Host Interactions with Bacterial Pathogens Study Section (HIBP)
Program Officer
Hiltke, Thomas J
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Texas Health Science Center San Antonio
Other Domestic Higher Education
San Antonio
United States
Zip Code
Hou, Shuping; Sun, Xin; Dong, Xiaohua et al. (2018) Chlamydial plasmid-encoded virulence factor Pgp3 interacts with human cathelicidin peptide LL-37 to modulate immune response. Microbes Infect :
Zhong, Guangming (2018) Chlamydia Spreading from the Genital Tract to the Gastrointestinal Tract - A Two-Hit Hypothesis. Trends Microbiol 26:611-623
Zhong, Guangming (2017) Chlamydial Plasmid-Dependent Pathogenicity. Trends Microbiol 25:141-152
Yang, Zhangsheng; Tang, Lingli; Shao, Lili et al. (2016) The Chlamydia-Secreted Protease CPAF Promotes Chlamydial Survival in the Mouse Lower Genital Tract. Infect Immun 84:2697-702
Lam, Tonika; Kulp, Dennis V; Wang, Rui et al. (2016) Small Molecule Inhibition of Rab7 Impairs B Cell Class Switching and Plasma Cell Survival To Dampen the Autoantibody Response in Murine Lupus. J Immunol 197:3792-3805
Conrad, Turner Allen; Gong, Siqi; Yang, Zhangsheng et al. (2016) The Chromosome-Encoded Hypothetical Protein TC0668 Is an Upper Genital Tract Pathogenicity Factor of Chlamydia muridarum. Infect Immun 84:467-79
Dai, Jin; Tang, Lingli; Chen, Jianlin et al. (2016) The p47phox deficiency significantly attenuates the pathogenicity of Chlamydia muridarum in the mouse oviduct but not uterine tissues. Microbes Infect 18:190-8
Dai, Jin; Zhang, Tianyuan; Wang, Luying et al. (2016) Intravenous Inoculation with Chlamydia muridarum Leads to a Long-Lasting Infection Restricted to the Gastrointestinal Tract. Infect Immun 84:2382-2388
Tang, Lingli; Chen, Jianlin; Zhou, Zhiguang et al. (2015) Chlamydia-secreted protease CPAF degrades host antimicrobial peptides. Microbes Infect 17:402-8
Sun, Xin; Yang, Zhangsheng; Zhang, Hongbo et al. (2015) Chlamydia muridarum induction of glandular duct dilation in mice. Infect Immun 83:2327-37

Showing the most recent 10 out of 51 publications