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Roger Rank, Ph.D.
Immunology/Bacteriology Research Interest: Immunology and pathogenesis of infections with Chlamydia Ph.D. Hahnemann University Phone: (501)
364-2474 Research Description Chlamydia trachomatis is the leading cause of sexually transmitted disease in the United States and Europe , with roughly 10% of the sexually active population infected. The organism produces a urethritis in males and cervicitis in women. Generally, the infection is asymptomatic in the female. While the primary target in female is the cervix, the organism may move up the genital tract and infect the fallopian tubes, producing salpingitis or pelvic inflammatory disease. The consequences of fallopian tube infection may be the development of scar tissue which can lead to tubal obstruction and infertility. In addition, C. trachomatis is the causative agent of trachoma, the leading cause of preventable blindness in the world. Our group has maintained an active and funded research program on the study of chlamydial infections for the last 33 years. During this time, we initially developed and characterized the guinea pig and mouse models for chlamydial genital infection and subsequently employed those models to describe the basic adaptive immune mechanisms elicited by the infection. In our studies, we have established an essential role for both antibody and cellular immune mechanisms in resolution of and resistance to genital disease and characterized those responses in the genital tract. While the vast majority of that work investigated the responses in the female, we have initiated and are conducting studies on the host response to chlamydial infection in the male genital tract. In addition, it is apparent that infection acquired by the female from the male by sexual transmission results in a shorter infection course, suggesting that there are factors involved in the male which can affect the response in the female. While the host response is involved in a protective immune response, it is also patently clear that chlamydial disease is also caused by the host response. The current hypothesis is that both the acute inflammatory response and the T cell response play important roles in the production of disease. Therefore, the major goal of our research program currently is to understand the basic mechanisms of disease in both the genital tract and eye. Using our animal models, we now have the ability to examine and define the molecular and cellular mechanisms in vivo that are initiated by infection and lead to the overall pathologic response. We have found that neutrophils enter the infected epithelium within 6 hours of infection, well before the organism has completed one cycle of replication which takes about 24 hours. We are currently using molecular and cellular techniques to define the molecular mechanisms by which chlamydiae initiate the production of chemokines which result in the production of the inflammatory reaction. We are also examining the exact cellular and molecular mechanisms by which neutrophils damage the local epithelium and how they may influence the development of the adaptive immune response, all within the first 24 hours of infection. These studies will lead to exciting new concepts on the host-pathogen interaction at its most basic level. References Prantner, D., Darville, T., Sikes, J.D. , Andrews, C.W. Jr , Brade, H., Rank, R.G., Nagarajan, U.M. Critical role for IL-1 b during Chlamydia muridarum genital infection and bacterial replication-independent secretion of IL-1 b in mouse macrophages. Infect. Immun. In press, 2009. Rank, R. G., Lacy, H. M., Goodwin, A. M., Sikes, J. D., Whittimore, J. Wyrick, P. B., Nagarajan, U. M.. Host chemokine and cytokine response in the endocervix within the first developmental cycle of Chlamydia muridarum . Infect. Immun. In press, 2009. Rank, R.G., Whittum-Hudson, J.A. Protective Immunity to Chlamydia: Evidence from Animal Studies. J. Infectious Diseases, supplement. In press, 2009. Tan, C., Hsia, R-c, Shou, H, Carrasco1, J.A., Rank, R.G., Bavoil, P.M. Variable expression of surface-exposed polymorphic membrane proteins in in vitro grown Chlamydia trachomatis. Cell. Microbiology. In press, 2009. Ramsey, K. H., Sigar, I. M., Schripsema, J. H., Denman, C. J., Bowlin, A. K., Myers, G. S. A., Rank, R.G. Strain and virulence diversity in the mouse pathogen Chlamydia muridarum. Infect. Immun. 77:3284-3293, 2009. Mallet, D.G., Heymer, Kelly-Jean, Rank, R.G., Wilson , D.P. Chlamydial infection and spatial ascension of the female genital tract: a novel hybrid cellular automata and continuum mathematical model. FEMS Immunol. Med. Microbiol. 57:173-182, 2009. Wilson , D.P., Bowlin, A.K., Bavoil, P.M., Rank, R.G . Ocular pathology elicited by Chlamydia and the predictive value of quantitative modeling. J. Infectious Diseases 199:1780-1789, 2009. Rank, R.G., Bowlin, A. K., Cané, S., Shou, H., Liu, Z., Nagarajan, U M., Bavoil, P. M. Effect of chlamydiaphage f CPG1 on the course of conjunctival infection with Chlamydia caviae in guinea pigs. Infection and Immunity, 77:1216-1221, 2009. Rank, R.G., Whittimore, J., Bowlin, A. K, Dessus-Babus, S., Wyrick, P. B. Chlamydiae and polymorphonuclear leukocytes: Unlikely allies in the spread of chlamydial infection. FEMS Immunol.Med. Microbiol. 54:104-114, 2008. Rank, R.G. The CD4 Response. In Chlamydia: Genomics, Pathogenesis and Implications for Control , Bavoil, P. and Wyrick, P. (eds). Horizon Bioscience, Norfolk , U.K. 2006. Burall, L.S., Liu, Z., Rank, R., Bavoil, P.M. The chlamydial invasion-like protein gene conundrum. Microbes and Infection 9: 873-880, 2007. Nagarajan, U.M., Ojcius, D.M., Stahl, L., Rank, R.G., Darville, T. Chlamydia trachomatis Induces Expression of IFN-{gamma}-Inducible Protein10 and IFN-{beta} Independent of TLR2 and TLR4, but Largely Dependent on MyD88. J. Immunol.175: 450-460, 2005.
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