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Joseph M. Carlin

Education

Ph.D. Microbiology, Michigan State University (1985)

B.S. Microbiology, Michigan State University (1978)

Biographical Information

Joseph Carlin was a post-doc at the University of Wisconsin-Madison before joining the faculty at ÍÃ×ÓÏÈÉú University in 1990. Since then, he serves as Director of the Mallory-Wilson Center, Chair of the Pre-health Advisory Committee, and Chair of the Institutional Biosafety Committee.

As Lead Departmental Advisor for Microbiology for 13 years, and chair of the College of Arts and Science Curriculum Committee for 8 years, he has gained experience with a wide range of advising issues as well as familiarity with faculty and degree programs across the university.

His research focuses on Chlamydia and the mechanisms by which it evades the immune response, and his teaching portfolio includes a non-majors course, Microorganisms and Human Disease and an upper-level course, Medical Bacteriology, for majors.

He and his wife Dawn have raised 3 children in Oxford, and all 3 are ÍÃ×ÓÏÈÉú graduates.

Research Interests

Chlamydia trachomatis is the leading bacterial sexually transmitted infection (STI) in the United States, with an estimated 3-5 million new cases per year, as well as the leading cause of preventable blindness worldwide. Furthermore, chlamydial STIs in 80% of women and 50% of men produce little to no symptoms, and thereby remain undetected and untreated. Unfortunately, untreated infection can lead to tubal infertility and ectopic pregnancy. Although these infections can be detected by screening sexually active individuals, widespread screening is not routinely performed. An effective alternative would be the development of a vaccine. However, traditional approaches to vaccine development have been unsuccessful, simply because we do not yet understand the immunobiology of Chlamydia. My research has been focused on gaining that understanding, such that we might someday be able to prevent chlamydial infection. Chlamydial infection triggers the production of a variety of immunomodulatory molecules, collectively known as cytokines. Interferon-gamma, a cytokine produced in response to infection, induces several antimicrobial mechanisms, including the breakdown of tryptophan by indoleamine dioxygenase (IDO). Activation of IDO rapidly depletes intracellular tryptophan, thereby starving tryptophan-dependent Chlamydia of an amino acid it requires for protein synthesis. While this works effectively in tissue culture, the fact that chlamydial infections are widespread and often asymptomatic suggests that Chlamydia are somehow evading this immunological defense mechanism.

Current Projects

• Use of fluorescent lipid probes for identification and sorting of Chlamydia-infected cells.
• Effect of ceramide on the activation of indoleamine 2,3 dioxygenase by interferon.
• Evaluation of the effects of ceramide and Chlamydia in caspase activation.

Selected Publications

• Shirey, K A., J.-Y. Jung, and J.M. Carlin. 2006. Up-regulation of interferon-γ receptor expression due to Chlamydia Toll-like receptor interaction does not enhance STAT-1 signaling. Infect. Immun. 74:6877-6884.
• Robinson, C.M., P.T. Hale, and J.M. Carlin. 2006. NF-κB contributes to indoleamine dioxygenase transcriptional synergy by IFN-γ and tumor necrosis factor-alpha. Cytokine 35: 53-61.
• Shirey, K-A., and J.M. Carlin. 2006. Chlamydiae modulation of IFNγ-, IL 1β-, and TNFα-receptor expression in HeLa cells. Infect. Immun. 74:2482-2486.
• Shirey, K-A., J-Y. Jung, G.S. Maeder, and J.M. Carlin. 2006. Upregulation of IFN-γ receptor expression influences IDO activation in epithelial cells. J. Interferon Cytokine Res. 26:53-62.
• Robinson, C.M., P T. Hale, and J.M. Carlin. 2005. The Role of IFN-γ and TNF-α responsive regulatory elements in the synergistic induction of indoleamine dioxygenase. J. Interferon Cytokine Res. 25:20-30. 
• Robinson, C.M., K A. Shirey, and J.M. Carlin. 2003. Synergistic transcriptional activation of indoleamine dioxygenase by interferon-γ and tumor necrosis factor-α. J. Interferon Cytokine Res. 23:413-421. 
• Babcock, T.A. and J.M. Carlin. 2000. Transcriptional activation of indoleamine dioxygenase by interleukin-1 and tumor necrosis factor-α in interferon-treated epithelial cells. Cytokine 12:588-594. 
• Currier, A.R., M.H. Ziegler, M.R. Riley, T.A. Babcock, V.P. Telbis, and J.M. Carlin. 2000. Tumor necrosis factor-alpha and lipopolysaccharide enhance interferon-induced antichlamydial indoleamine dioxygenase activity independently. J. Interferon Cytokine Res. 20:369-370. 

More publications can be viewed on the .