For Federal Express:
1985-1991: Ph.D. in Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia, MO.
1991-1994: Post-doctoral Fellow, Division of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
1994-2012: Assistant, Associate and Full Professor, Department of Microbiology, QCOM, ETSU, Johnson City, TN.
1997: Visiting Professor and collaborator on program project entitled “Molecules and Mechanisms of Inflammatory Processes.” Reumaklinik Bad Bramstedt, Medical University of Lübeck, Lübeck, Germany.
2000, 2001: Visiting Lecturer in “Medical Microbiology-Virology”. University of South Dakota College of Medicine, Vermillion, SD, USA.
2012: Visiting Professor and collaborator. Institute of Pathology, Vetsuisse, University of Zurich, Zurich, Switzerland.
2015: Vice Chair of Education, Department of Biomedical Sciences, QCOM, ETSU, Johnson City, TN.
1. Regulation of chlamydial development in culture and in vivo.
2. Persistent chlamydial infection and pathogenesis.
3. Pathogenesis of co-infections.
Current Research Projects:
My Ph.D. and post-doctoral training was in the molecular and cellular biology of murine parvoviruses and ovine lentiviruses, respectively. However, my laboratory is now focused on sexually transmitted diseases of humans. Because sexually transmitted diseases cause enormous morbidity and mortality world wide, these studies have the potential to significantly impact human health. Our overall goal is to understand how the sexually transmitted bacterium, Chlamydia trachomatis, interacts with the host to produce disease. C. trachomatis is an obligate intracellular, Gram negative bacterium with a complex developmental cycle (Fig. 1). Genital
infections are very common in the US
, with greater than 2,800,000 new cases being reported each year. Chlamydial infection is often inapparent and can persist for years, causing diseases ranging from mild inflammation to infertility or life-threatening ectopic pregnancy. It is our hope that a better understanding of chlamydial pathogenesis will ultimately lead to the development of more effective therapies and preventative interventions.
We currently have two main research projects ongoing in our laboratory. The first project is entitled “Development of an animal model of chlamydial persistence”; NIAID R21 AI082322-01; 06/01/09-05/31/12), we are testing the following two hypotheses: i) amoxicillin-exposed, persistent chlamydiae can induce alterations in murine host cell gene expression; and ii) amoxicillin-exposure can induce persistent (i.e. viable but non-infectious) chlamydial infection in vivo. In the course of these studies, we have: i) definitively demonstrated that viable but non-infectious chlamydial forms are present in vivo under appropriate conditions; and ii) developed the first experimentally tractable animal model of chlamydial persistence. This unique model will ultimately facilitate exploration of how persistent infection impacts chlamydial pathogenesis, transmission and antimicrobial therapy.
The second project (“Characterization of a novel host pathway that regulates chlamydial development”) was previously supported by NIH/NIAID R21AI59563 and is now supported by NIH/NIAID R01 AI095637. Previously published data from our laboratory demonstrate that HSV-2 super-infection of C. trachomatis-infected, human genital epithelial cells profoundly alters chlamydial development. In the course of exploring this co-infection model, we discovered that the host cell surface protein nectin-1 is a host regulator of chlamydial development. We are currently characterizing this novel host regulator by studying chlamydia replication in nectin-1 knockout cells and following the progression of genital tract disease in vaginally-infected nectin-1 knockout mice. In a separate branch of this project, we have also recently demonstrated that vaginal C. muridarum infection can protect mice against a subsequent lethal herpes simplex virus challenge. We are currently dissecting the molecular mechanisms underlying this protection. Given that C. trachomatis/HSV co-infections are common and that the consequences of such co-infections are unstudied, our studies will reveal new and interesting facets of HSV/chlamydia co-pathogenesis and will hasten development of in vivo models of polymicrobial sexually transmitted infections.
As basic medical sciences educators, we have four tasks. First, we must decide what, from the immense medical/research literature, to teach. Second, we have to present course material in such a way that the majority of our students can comprehend it. Third, we must evaluate how well the students have mastered the subject. Fourth, we must motivate our students to learn the material. All four tasks are difficult and must be mastered if one is to be an effective educator. Basic scientists tend to be most comfortable with those tasks that are quantifiable. Thus, motivation, a fuzzy subject at best, is usually left up to the students and is addressed, at most, by giving a course grade. In my opinion, the issue of motivation is paramount. Motivated students will ALWAYS accomplish more than those that are unmotivated, regardless of other factors. Although we have little ability to determine why our students decided to become physicians or scientists, we can substantially influence their motivation once they enter our medical and graduate programs. So, once they are here, how do we help keep them motivated? Though professional expectations and grades play a role, I would suggest that an often overlooked requirement is respect. If a faculty member puts effort into their teaching, most students will respect them for it. Such respect provides the students with additional motivation; making them more likely to listen, work hard and perform. Such respect is not given freely, it is earned by the efforts an instructor makes on behalf their students. I honestly feel that, because it is my job, I have a responsibility to my students and to the people of Tennessee to teach to the best of my ability. This means that if I do not currently have all the necessary skills, it is my responsibility to acquire them - a task that I take very seriously.
I have always considered direction of student research projects and service on student advisory committees to be a critical component of my position in the College of Medicine. One of the most important considerations in designing a student research project is that it must provide a complete, well‑rounded scientific education. All of my students engage in projects that require a wide range of knowledge and experimental approaches/techniques. These projects encourage the student to: i) become proficient in many different experimental approaches, ii) develop independence and tenacity, iii) develop the ability to properly design and trouble‑shoot experiments, iv) learn how to "ask the right questions" and v) stay current in the scientific literature. These abilities will allow students to successfully compete for jobs and develop independent careers.
Former and Current Students:
Graduate Research Students:
Lillia Holmes, M.S., Aug. 1997.
Michelle Abelson, M.S., May 1998.
Michelle Abelson, Ph.D., Dec. 2000.
Bridget Graves, M.S., Dec. 2001.
Srilekha (Rinti) Deka, Ph.D., Dec. 2005.
Jennifer Vanover-Hall, Ph.D., Dec. 2008.
Jingru Sun, Ph.D., May 2009.
Reginia Phillips-Campbell, Ph.D. Dec. 2013.
Jessica Slade, current Ph.D. student.
Undergraduate Research Students:
Elizabeth Hanson, B.S., May 2001. (University Honors Scholar)
Sarah Mullins, B.S., May 2009. (Midway Honors Scholar)
Marissa Bambino, B.S., May 2012.
Matt Novak, B.S., May 2012.
Julia Colgrove, B,S. May 2014. (University Honors Scholar)
Hena Yakoob, B.S., May 2015. (University Honors Scholar)
Matthew Grimm, Summer 2015. (Niswonger Scholar)
McNair Program Research Students:
Nicole Mikel, Summer 1996.
Eric Donald, Summer 1997.
Chris Daniels, Fall/Spring 2008-9.
Medical Student Summer Research Fellows:
Ritu Khanna, COM Class of 2005.
Dawn Lajoie, COM Class of 2006.
Scott Embry, COM Class of 2010.
Courtney Childress, COM Class of 2014.
Student Honors and Awards (since 2001):
1. Elizabeth Hansen (Undergraduate Honors student). Awarded:
2. Srilekha Deka (Ph.D. student). Awarded:
4. Jennifer Vanover (Ph.D. student). Awarded:
5. Chris Daniels (Undergraduate McNair student). Awarded:
6. Regenia Phillips-Campbell (Ph.D. student). Awarded:
7. Matthew Novak (Undergraduate student). Awarded:
8. Jessica Slade (Ph.D. student). Awarded:
NIH/NIAID R01 AI095637- "Characterization of a novel host pathway that regulates chlamydial development." 08/17/11-07/31/16.
Jennifer Kintner – research technician and lab mom.
Jessica Slade – Ph.D. student
1. Vanover J, Kintner J, Whittimore J, Schoborg RV. Interaction of herpes simplex virus type 2 (HSV-2) glycoprotein D with the host cell surface is sufficient to induce Chlamydia trachomatis persistence. Microbiology. 2010 May;156(Pt5):1294-302. doi: 10.1099/mic.0.036566-0. Epub 2010 Jan 28. PubMed PMID: 20110302; PubMed Central PMCID: PMC2889450.
2. Schoborg RV. Chlamydia persistence -- a tool to dissect chlamydia—host interactions. Microbes Infect. 2011 Jul;13(7):649-62. doi: 10.1016/j.micinf.2011.03.004. Epub 2011 Mar 31. Review. PubMed PMID: 21458583; PubMed Central PMCID: PMC3636554.
3. Phillips Campbell R, Kintner J, Whittimore J, Schoborg RV. Chlamydia muridarum enters a viable but non-infectious state in amoxicillin-treated BALB/c mice. Microbes Infect. 2012 Nov;14(13):1177-85. doi: 10.1016/j.micinf.2012.07.017. Epub 2012 Aug 23. PubMed PMID: 22943883; PubMed Central PMCID: PMC3654801.
4. Leonard CA, Schell M, Schoborg RV, Hayman JR. Encephalitozoon intestinalis infection increases host cell mutation frequency. Infect Agent Cancer. 2013 Nov 4;8(1):43. doi: 10.1186/1750-9378-8-43. PubMed PMID: 24188884; PubMed Central PMCID: PMC4174903.
5. Phillips-Campbell R, Kintner J, Schoborg RV. Induction of the Chlamydia muridarum stress/persistence response increases azithromycin treatment failure in a murine model of infection. Antimicrob Agents Chemother. 2014;58(3):1782-4. PubMed PMID: 24342653; PubMed Central PMCID: PMC3957849.
6. Kintner J, Lajoie D, Hall J, Whittimore J, Schoborg RV. Commonly prescribed β-lactam antibiotics induce C. trachomatis persistence/stress in culture at physiologically relevant concentrations. Front Cell Infect Microbiol. 2014 Apr 11;4:44. doi: 10.3389/fcimb.2014.00044. eCollection 2014. PubMed PMID: 24783061; PubMed Central PMCID: PMC3990100.
7. Borel N, Pospischil A, Hudson AP, Rupp J, Schoborg RV. The role of viable but non-infectious developmental forms in chlamydial biology. Front Cell Infect Microbiol. 2014 Jul 24;4:97. doi: 10.3389/fcimb.2014.00097. eCollection 2014. PubMed PMID: 25105096; PubMed Central PMCID: PMC4109588.
8. Hall JV, Sun J, Slade J, Kintner J, Bambino M, Whittimore J, Schoborg RV. Host nectin-1 is required for efficient Chlamydia trachomatis serovar E development. Front Cell Infect Microbiol. 2014 Nov 6;4:158. doi: 10.3389/fcimb.2014.00158. eCollection 2014. PubMed PMID: 25414835; PubMed Central PMCID: PMC4222120.
9. Kintner J, Schoborg RV, Wyrick PB, Hall JV. Progesterone antagonizes the positive influence of estrogen on Chlamydia trachomatis serovar E in an Ishikawa/SHT-290 co-culture model. Pathog Dis. 2015 Jun;73(4). pii: ftv015. doi: 10.1093/femspd/ftv015. Epub 2015 Feb 26. PubMed PMID: 25724891.
I am a firm believer in the adage “work hard and play hard”. Most of my “out of work” activities are of the athletic variety and include backpacking, canoeing, kayaking, camping, fishing and wildlife photography.