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Christopher M. Reilly, Ph.D.
Associate Professor / Discipline Chair for Physiology
Edward Via Virginia College of Osteopathic Medicine
2265 Kraft Drive, Blacksburg, VA 24060
Tele: 540-231-5345
Fax: 540-231-5252
Email:creilly@vcom.vt.edu |
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Discipline: |
Physiology |
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Education: |
| 1991 |
University of New Mexico |
B.S. |
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| 1997 |
Medical College of Georgia |
Ph.D. |
| 2000 |
Medical University of South Carolina |
Post Doctoral Research Fellowship |
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Currently Teaching: |
Endocrine, reproduction and renal physiology |
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Current Research: |
The etiology of systemic lupus erythematosus (SLE) remains an enigma although genetic factors influenced by environmental agents appear to trigger the disease. Studies of inflammatory diseases and specifically lupus nephritis are enhanced by the availability of murine models. One such model of SLE is the MRL/lpr mouse. Autoantibodies produced by these mice are similar in spectrum to those seen in human lupus including anti-double stranded DNA antibodies and anti-Sm antibodies. MRL/lpr mice develop glomerulonephritis and vasculitis at an early age (4-5 months). In MRL/lpr lupus mice, kidney infiltrating T cells secrete IFN-gamma, which in turn, induces the expression of CSF-1 and TNF-alpha within the kidney recruiting monocytes and activating resident glomerular mesangial cells to produce cytokines and inflammatory mediators such as IL1beta, TNF-alpha, IL-12, reactive oxygen species, and nitric oxide (NO). The ongoing IFN-gamma mediated inflammation in proliferative lupus nephritis suggests that targeting downstream effects of IFN-gamma e.g. IRF-1 and IFR-2 may prevent macrophage and mesangial cell activation and suppress the inflammatory cascade observed in lupus nephritis. Using MRL/lpr mice we target signal transduction pathways responsible for the inflammatory response to determine the effect of targeting specific genes to elucidate the inflammatory cascade. In another project we have identified a group of compounds, histone deacetylase inhibitors (HID's), that act to inhibit cell proliferation and activation. Using our MRL/lpr mouse model, we are examining the efficacy of HDI administration for the treatment in lupus nephritis. |
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Current Academic and Clinical Service: |
Currently teaching autoimmunity at Virginia Tech Graduate School |
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Graduate and Medical School Advisor |
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Professional and Community Activities: |
Via Wellness |
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Special Olympics |
