Daniel D. Rockey, PhD
Associate Professor
e-mail:rockeyd@orst.edu
website:http://oregonstate.edu/~rockeyd/
Interests
Chlamydia
Pathogenesis Disease
Sexually Transmitted Disease
Trachoma
Cell Biology
PhD 1989 Oregon State University Research
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.
Selected Publications
Rockey DD, W Viratyosin, JP Bannantine, RJ Suchland, and WE Stamm. 2002. Diversity within inc genes of clinical Chlamydia trachomatis variant isolates that occupy non-fusogenic inclusions. Microbiology 148:2497-2505.
Rockey DD, MA Scidmore, JP Bannantine, and WJ Brown. 2002. Proteins in the chlamydial inclusion membrane. Microbes and Infection 4:333-340.
Geisler WM, RJ Suchland, DD Rockey, and WE Stamm. 2001. Epidemiology and clinical manifestations of unique Chlamydia trachomatis isolates that occupy nonfusogenic inclusions. Journal of Infectious Diseases 184:879-884.
Lenart J, AA Andersen, and DD Rockey. 2001. Growth and development of tetracycline-resistant Chlamydia suis. Antimicrobial Agents and Chemotherapy 45:2198-2203.
Bannantine, JP, RS Griffiths, W Viratyosin, WJ Brown, and DD Rockey. 2000. A secondary structure motif predictive of protein localization to the chlamydial inclusion membrane. Cellular Microbiology 2:35-47.
Rockey, DD, J Lenart, and RS Stephens. 2000. Genome sequencing and out understanding of chlamydiae. Infection and Immunity 68:5473-5479.
Brown, WJ and DD Rockey. 2000. Identification of an antigen localized to an apparent septum within dividing chlamydiae. Infection and Immunity 68:708-715.
Suchland, RJ, JP Bannantine, DD Rockey and WE Stamm. 2000. Isolates of Chlamydia trachomatis that occupy nonfusogenic inclusions lack IncA, a protein localized to the inclusion membrane. Infection and Immunity 68:360-367.
Bannantine, JP and DD Rockey. 1999. Use of a primate model system to identify Chlamydia trachomatis protein antigens recognized uniquely in the context of infection. Microbiology 145:2077-2085.