Roger G. Rank, PhD
Professor Microbiology & Immunology, University of Arkansas for Medical Sciences, College of Medicine
Phone: (501) 364-2474

The Chlamydia Research Group has maintained an active and funded research program on the study of chlamydial infections for the last 30 years. During this time, the program 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. Their studies 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, the laboratory has initiated and is 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 the research program currently is to understand the basic mechanisms of disease in both the genital tract and eye.

Using their animal models, the Chlamydia Research Group now has 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. They 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. Currently, they are 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. They 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.

Rank, R.G., Bowlin, A.K., Tormanen, K. I., Wang, Y., Maurelli, A. T. Effect of the inflammatory response upon the in vivo competition between two chlamydial variants in the guinea pig model of inclusion conjunctivitis. Infect. Immun. 80:612-619, 2012

Rank RG, Whittimore J, Bowlin AK, Wyrick PB. In vivo ultrastructural analysis of the intimate relationship between polymorphonuclear leukocytes and the chlamydial developmental cycle. Infect Immun. 2011 Aug;79(8):3291-301. Epub 2011 May 16.

Carrasco JA, Tan C, Rank RG, Hsia RC, Bavoil PM. Altered developmental expression of polymorphic membrane proteins in penicillin-stressed Chlamydia trachomatis. Cell Microbiol. 2011 Jul;13(7):1014-25. Epub 2011 Apr 26.

Lacy HM, Bowlin AK, Hennings L, Scurlock AM, Nagarajan UM, Rank RG. Essential role for neutrophils in pathogenesis and adaptive immunity in Chlamydia caviae ocular infections. Infect Immun. 2011 May;79(5):1889-97. Epub 2011 Mar 14.

Saraswati S, Block AS, Davidson MK, Rank RG, Mahadevan M, Diekman AB. Galectin-3 is a substrate for prostate specific antigen (PSA) in human seminal plasma. Prostate. 2011 Feb 1;71(2):197-208.

Rank RG, Whittum-Hudson JA. Protective immunity to chlamydial genital infection: evidence from animal studies. J Infect Dis. 2010 Jun 15;201 Suppl 2:S168-77. Review.

Wang Y, Nagarajan U, Hennings L, Bowlin AK, Rank RG. Local host response to chlamydial urethral infection in male guinea pigs. Infect Immun. 2010 Apr;78(4):1670-81. Epub 2010 Feb 1.

Binet R, Bowlin AK, Maurelli AT, Rank RG. Impact of azithromycin resistance mutations on the virulence and fitness of Chlamydia caviae in guinea pigs. Antimicrob Agents Chemother. 2010 Mar;54(3):1094-101.

Tan C, Hsia RC, Shou H, Carrasco JA, Rank RG, Bavoil PM. Variable expression of surface-exposed polymorphic membrane proteins in in vitro-grown Chlamydia trachomatis. Cell Microbiol. 2010 Feb;12(2):174-87. Epub 2009 Oct 6.

Rank RG, Lacy HM, Goodwin A, Sikes J, Whittimore J, Wyrick PB, Nagarajan UM. Host chemokine and cytokine response in the endocervix within the first developmental cycle of Chlamydia muridarum. Infect Immun. 2010 Jan;78(1):536-44. Epub 2009 Oct 19.

*To find additional publications by this author, please visit Pubmed Central, a National Institutes of Health-operated site for electronic distribution of life sciences research reports.

Eco-pathogenomics of Chlamydia reproductive tract infection. U19 AI084044-01 NIAID, NIH; 07/01/09 – 06/30/14; Director, Animal Model Core.

Role of the neurogenic inflammatory pathway in the genital tract immune response. R21AI83422-1, NIAID, NIH; 06/05/09 – 05/31/12; Principal Investigator.

Chlamydia as a Gut Commensal: A Reservoir for Reinfection of the Genital Tract. Arkansas Children’s Hospital Research Institute/Arkansas Biosciences Institute; 11/01/11 – 10/31/12; Co-Principal Investigator.

Development and Characterization of a Model to Study the Innate Response to Chlamydial Genital Infection Independent of the Adaptive Immune Response. Arkansas Children’s Hospital Research Institute/Arkansas Biosciences Institute; 11/01/10 – 04/30/12; Principal Investigator.