Kyle H. Ramsey, Ph.D.

Professor of Microbiology and Immunology / Dean of Basic Science

Midwestern University
Chicago College of Osteopathic Medicine
(Secondary appointments: CDMI, CVM)
Microbiology and Immunology, Basic Science Division
Auditorium Building, Room #562
555 31st St.
Downers Grove, IL 60515
Office: (630) 515-6175



B.A. Biology Ouachita Baptist University 1982
Ph.D. Microbiology amd Immunology University of Arkansas for Medicine 1990


Infectious diseases, immunology, immunopathological basis of disease caused by pathogens of the genus: Chlamydia

Chlamydial infections are ubiquitous in humans and animals.  In the U.S. and other industrialized societies, selected strains of Chlamydia trachomatis cause sexually transmitted infections that lead to pelvic inflammatory disease, tubal factor infertility and ectopic pregnancy.  In the less-developed world a different set of C. trachomatis strains cause the most common form of infectious blindness, trachoma, from which the species derives its name. In these areas, rather than sexual transmission, key environmental factors are involved in transmission. C. pneumoniae is a common respiratory infection in humans and has also been linked to several chronic disease states. C. psittaci infections cause ocular, respiratory, urogenital and gastrointestinal disease in domestic animals and wildlife and may cross the species barrier and cause infection in humans.

My laboratory is dedicated to discovering how chlamydial agents induce inflammatory damage in humans and animals and how best protective immunity can be accomplished so that we may someday derive a safe and efficacious vaccine.  Most of our work is accomplished through the lens of a mouse model. However, our long-term plans include extension of our findings for application in companion and food animals, wildlife and eventually humans.  We actively pursue partnerships in this regard and currently have collaborations in the U.S., U.K., Australia and India.

Selected Research Projects

Project I:  The role of the chlamydial plasmid in pathogenesis and immunity in a mouse model.  Both C. trachomatis and C. muridarum are known to routinely carry a plasmid. For many years, the role of this plasmid in establishing infection, eliciting immunity and/or causing disease was unknown.  It has more recently been shown that the plasmid moderates infectivity and phenotype in vitro (cell culture) and virulence in vivo - in the mouse (and presumably in human infections).  We seek to understand how the plasmid effects virulence, affects chromosomal gene expression, and elicits immunological protection. Our current collaborations on this project include the laboratories of Professor Ian N. Clarke (the University of Southampton School of Medicine, Southampton, U.K.) and Dr. Ashlesh K. Murthy (Midwestern University, U.S.A.).

Project II:  Using chlamydial genomic variants to understand chlamydial immunity and pathogenesis.  We have shown that, like all bacteria, the genome of chlamydia exhibits spontaneous mutation as a natural process. We have more recently shown that many genomic variants exist within two commonly used strains of C. muridarum. These variations are in the form of small or single nucleotide polymorphisms (1, 2 or 3 base pair additions, substitutions or deletions).  We believe that some of these mutations may lead to attenuation of virulence while in culture thereby weakening the pathogen when introduced into the mouse host.  In this Project, our aim is to cross-map the chlamydial genes responsible for virulence with the host genes associated with resistance and susceptibility.  When accomplished, we believe that we will be able to identify critical host and pathogen genes. The interface of these genes will point us to a greater understanding of why some people develop chronic disease states following chlamydial infection and others develop a protective immune response.  The results will have a direct impact on development of an efficacious chlamydial vaccine.  Our collaborators on this project include Drs. Jan Peters and Gerry Byrne (University of Tennessee Health Sciences Center) and the Regional Biocontainment Laboratory in Memphis, Tennessee.

Project III:  Inflammation and pathogenesis in chlamydial infection.  In this project we explore the molecular mechanisms that induce inflammatory damage during chlamydial infections.  Many labs throughout the world are currently studying inflammatory mechanisms and "signaling cascades" in chlamydial infection.  These effectors and effector pathways (e.g. cytokines and chemokines) are important in understanding the "come hither" mechanisms that elicit inflammatory damage during and immediately following a chlamydial infection.  Rather further study studying signaling, our lab has focused on the mechanisms, downstream of the signaling, that actually affect tissue damage.  We have shown, for example, that innate mechanisms such as oxygen free radicals and matrix metalloproteinases contribute significantly to the damage that occurs during chlamydial infection and further postulate that other mechanisms are also at play. We now work with the Murthy Lab at Midwestern University to understand the adaptive immune mechanisms mediated by CD8+ T lymphocytes later in infection and how innate and adaptive mechanism are elicited together to result in chlamydia infection-associated immunopathology.  Understanding how the damage occurs will help us to derive a vaccine that is both safe and efficacious.

The mouse as a model for the study of human pelvic inflammatory disease of chlamydial etiology (Project III).  Panel A and B: Oviduct (arrows), uterus ("U") and ovary ("O") of an uninfected mouse (Panel A) or a mouse at 14 days post-infection with Chlamydia muridarum (Panel B). Panel C and D:  Hematoxylin and eosin stained histological sections of the oviduct  shown in Panels A and B.  The lumen (L) of the oviduct  from the uninfected mouse (Panels A and C) is patent and plicae are intact.  The oviduct  from the infected mouse is inflamed with acute and chronic inflammatory cells occluding the lumen (L) and plicae are destroyed (Panel D). The image on the far right is a frozen cross section of an inflamed oviduct stained using fluorescence immunohistochemistry for matrix metalloproteinase-9 (MMP-9).  MMP-9 is stained red/pink and cell nuclei are stained blue.  The section depicts the accumulation of acute inflammatory cells elaborating MMP-9 (arrows) at the basolateral surface of the epithelium (E) and some inflammatory cells are undergoing transepithelial migration into the lumen.  The cells seem to discharge MMP-9 as they migrate across the infected epithelial layer and linto the lumen of the oviduct becasue the cells in the lumen have reduced MMP-9 staining.  We believe MMP-9 is responsible for a siginficant portion of the tissue destruction that occurs during infection in this model. 

Selected Publications


Winstanley CE, Ramsey KH, Marsh P, Clarke IN. Development of an enzyme-linked immunosorbent assay for the detection of antibodies to a common urogenital derivative of Chlamydia trachomatis plasmid-encoded PGP3 . J Immunol Methods. 2017 Jun;445:23-30. doi: 10.1016/j.jim.2017.03.002. Epub 2017 Mar 7.  PMID: 28283408


Murthy AK, Li W, Ramsey KH.  Immunopathogenesis of Chlamydial infections.  Curr Top Microbiol Immunol. 2016 Jul 2. [Epub ahead of print] PMID: 27370346

Ramsey KH, Sigar IM, Schripsema JH, Townsend KE, Barry RJ, Peters J, Platt KB. Detection of Chlamydia infection in Peromyscus species rodents from sylvatic and laboratory sources. Pathog Dis. 2016 Apr;74(3). pii: ftv129. doi: 10.1093/femspd/ftv129. Epub 2016 Jan 4.  PMID: 26733499.

Vlcek KR, Li W, Manam S, Zanotti B, Nicholson BJ, Ramsey KH, Murthy AK.  The contribution of Chlamydia-specific CD8+ T cells to upper genital tract pathology.  Immunol Cell Biol. 2016 Feb;94(2):208-12. doi: 10.1038/icb.2015.74. Epub 2015 Sep 1.  PMID: 26323581.

Zafiratos, MT, Manam, S, Henderson, KKRamsey, KH, Murthy, AK.  CD8+ T cells mediate Chlamydia pneumoniae-induced atherosclerosis in mice. Pathog Dis. 2015 Oct;73(7). pii: ftv052. doi: 10.1093/femspd/ftv052. Epub 2015 Jul 27.  PMID: 26220574.


Jasper DK, Sigar IM, Schripsema JH, Sainvil CK, Smith CL, Yeruva L, Rank RG,Murthy AK, Widder JR, Ramsey KH.  Genomic variant representation in a Chlamydia population is dynamic and adaptive with dependence on in vitro and in vivo passage. Pathog Dis. 2015 Feb;73(1):1-12. doi: 10.1093/femspd/ftv003. Epub 2015 Jan 28. PubMed PMID: 25673672.


Manam S, Thomas JD, Li W, Maladore A, Schripsema JH, Ramsey KH, Murthy AK. Tumor Necrosis Factor (TNF) Receptor Superfamily Member 1b on CD8+ T Cells and TNF Receptor Superfamily Member 1a on Non-CD8+ T Cells Contribute Significantly to Upper Genital Tract Pathology Following Chlamydial Infection. J Infect Dis. 2014 Dec 30. pii: jiu839. [Epub ahead of print] PubMed PMID: 25552370.

Ramsey, KH, Schripsema JH, Smith BJ, Wang Y, Jham BC, O'Hagan KP, Thomson NR, Murthy AK, Skilton RJ, Chu P, Clarke IN. Plasmid CDS5 influences infectivity and  virulence in a mouse model of Chlamydia trachomatis urogenital infection. Infect Immun. 2014 Aug;82(8):3341-9. doi: 10.1128/IAI.01795-14. Epub 2014 May 27. PubMed PMID: 24866804; PubMed Central PMCID: PMC4136204.

Wang Y, Cutcliffe LT, Skilton RJ, Ramsey KH, Thomson NR, Clarke IN. The genetic basis of plasmid tropism between Chlamydia trachomatis and Chlamydia muridarum. Pathog Dis. 2014 Oct;72(1):19-23. doi: 10.1111/2049-632X.12175. Epub 2014 May 8. PubMed PMID: 24700815; PubMed Central PMCID: PMC4314687.

Andrew DW, Cochrane M, Schripsema JH, Ramsey KH, Dando SJ, O'Meara CP, Timms P, Beagley KW. The duration of Chlamydia muridarum genital tract infection and associated chronic pathological changes are reduced in IL-17 knockout mice but protection is not increased further by immunization. PLoS One. 2013 Sep 20;8(9):e76664. doi: 10.1371/journal.pone.0076664. eCollection 2013. PubMed PMID: 24073293; PubMed Central PMCID: PMC3779189.

Sigar IM, Schripsema JH, Wang Y, Clarke IN, Cutcliffe LT, Seth-Smith, HM, Thomson NR, Bjartling C, Unemo M, Persson K, Ramsey KH. Plasmid deficiency in urogenital isolates of Chlamydia trachomatis reduces infectivity and virulence in a mouse model. Pathog Dis. 2014 Feb;70(1):61-9. doi: 10.1111/2049-632X.12086. Epub 2013 Sep 10. PubMed PMID: 24022847; PubMed Central PMCID: PMC4300952.


Tiwari V, Maus E, Sigar IM, Ramsey KH, Shukla D. Role of heparan sulfate in sexually transmitted infections. Glycobiology. 2012 Nov;22(11):1402-12. doi: 10.1093/glycob/cws106. Epub 2012 Jul 6. Review. PubMed PMID: 22773448; PubMed Central PMCID: PMC3481906.


Lee HY, Schripsema JH, Sigar IM, Lacy SR, Kasimos JN, Murray CM, Ramsey KH. A role for CXC chemokine receptor-2 in the pathogenesis of urogenital Chlamydia muridarum infection in mice. FEMS Immunol Med Microbiol. 2010 Oct;60(1):49-56. doi: 10.1111/j.1574-695X.2010.00715.x. PubMed PMID: 20602634.

Miyairi I, Ramsey KH, Patton DL. Duration of untreated chlamydial genital infection and factors associated with clearance: review of animal studies. JInfect Dis. 2010 Jun 15;201 Suppl 2:S96-103. doi: 10.1086/652393. Review. PubMed PMID: 20470047.

Dixon RE, Ramsey KH, Schripsema JH, Sanders KM, Ward SM. Time-dependent disruption of oviduct pacemaker cells by Chlamydia infection in mice. Biol Reprod. 2010 Aug 1;83(2):244-53. doi: 10.1095/biolreprod.110.083808. Epub 2010 Apr 28. PubMed PMID: 20427758; PubMed Central PMCID: PMC2907286.

Lee HY, Schripsema JH, Sigar IM, Murray CM, Lacy SR, Ramsey KH. A link between neutrophils and chronic disease manifestations of Chlamydia muridarum urogenital infection of mice. FEMS Immunol Med Microbiol. 2010 Jun 1;59(1):108-16. doi: 10.1111/j.1574-695X.2010.00668.x. Epub 2010 Mar 10. PubMed PMID: 20370824.