- Future Students
- Current Students
- Faculty & Staff
Daniel D. Rockey
Professional and Research Interests:
- Sexually Transmitted Disease
- Cell Biology
Interactions Between Chlamydiae and The Mammalian Host.
The four species of chlamydiae are obligate intracellular bacteria that cause disease in a wide variety of animal species. In humans, Chlamydia trachomatis and C. pneumoniae cause a variety of diseases of the eye, genital tract and lung. These conditions affect millions of people worldwide and lead to billions of dollars in medical expenses yearly in the U.S. alone. Additionally, chlamydial etiology has been postulated for certain types of arthritis and, most surprisingly, arterial sclerosis. Although the host range and diseases caused by the chlamydiae are diverse, the infectious process used by all chlamydiae is very similar. All chlamydiae have an alternating life cycle consisting of two distinct developmental forms. Attachment to and entry into the host cell is mediated through a non-metabolic life stage, the elementary body (EB), while intracellular multiplication progresses through the reticulate body (RB), a metabolically active, non-infectious form. After EB attachment and entry, chlamydiae remain separated from the cytoplasm in a membrane-bound vesicle, which grows in size until cell lysis and bacterial release. Fusion of the inclusion with host cell lysosomes is specifically inhibited during infection by chlamydiae- a process that protects the invading bacterium from the toxic environment within the lysosome. Conversely, fusion of the inclusion with Golgi derived vesicles is an integral part of the developmental process and it is thought this pathway may deliver nutrients to the growing chlamydiae. A final twist in this story is that early chlamydial protein synthesis is required for the placement of the inclusion into the appropriate vesicle trafficking pathway. Very little is known of the molecular events leading to these processes.
Our laboratory group focuses on mechanisms used by chlamydiae to develop and maintain the inclusion. We (and others) have identified a collection of proteins- termed Inc proteins- that are localized to the inclusion membrane of infected cells. Each of these proteins is present in Chlamydia -infected tissue culture cells but absent in the purified elementary bodies. Additionally, IncA is exposed to the cytoplasm of infected cells and is phosphorylated by host cell protein kinases. These data are exciting because they show Inc proteins to be potentially very important in the unique interactions between host cells and chlamydiae. We hope to use these lines of investigation to further our understanding of the cellular processes parasitized by chlamydiae during infection, and possibly to identify ways to interfere with this parasitism.
Visit PubMed for a full list of Dr. Rockey's Publications.
Su H, Raymond L, Rockey DD, Fischer E, Hackstadt T, Caldwell HD. 1996. A recombinant Chlamydia trachomatis major outer membrane protein binds to heparan sulfate receptors on epithelial cells.. Proceedings of the National Academy of Sciences of the United States of America. 93(20):11143-8.
Rockey DD, Chesebro BB, Heinzen RA, Hackstadt T. 1996. A 28 kDa major immunogen of Chlamydia psittaci shares identity with Mip proteins of Legionella spp. and Chlamydia trachomatis-cloning and characterization of the C. psittaci mip-like gene.. Microbiology (Reading, England). 142 ( Pt 4):945-53.
Hackstadt T, Scidmore MA, Rockey DD. 1995. Lipid metabolism in Chlamydia trachomatis-infected cells: directed trafficking of Golgi-derived sphingolipids to the chlamydial inclusion.. Proceedings of the National Academy of Sciences of the United States of America. 92(11):4877-81.
Yuan Y, Lyng K, Zhang YX, Rockey DD, Morrison RP. 1992. Monoclonal antibodies define genus-specific, species-specific, and cross-reactive epitopes of the chlamydial 60-kilodalton heat shock protein (hsp60): specific immunodetection and purification of chlamydial hsp60.. Infection and immunity. 60(6):2288-96.