Lee J. Quinton, Ph.D.

Assistant Professor of Medicine and Pathology

quintonCollege Education: University of Southern Mississippi, B.S., 1999
Graduate School: Louisiana State University Health Sciences Center, Ph.D., 2003
Post-Doctoral Fellowships:

  • Louisiana State University Health Sciences Center, 2004 (Pulmonary Host Defense. Gregory J. Bagby Ph.D. and Steve Nelson M.D.)
  • Harvard School of Public Health, 2005-2008 (Pulmonary Host Defense, Joseph P. Mizgerd, Sc.D.)

Special Interests:

  • Pneumonia
  • The acute phase response
  • Cytokine regulation
  • Acute lung injury

Lung infections account for a tremendous burden of disease, representing the most frequent cause of infection-related deaths and a common cause of acute lung injury. The innate immune response is critical for the prevention of lower respiratory tract infections. Yet, this response must be tightly regulated, such that adequate host defenses do not result in inflammatory lung injury.

Our long-term goal is to elucidate intra- and extra-pulmonary signaling events required for an immune response that is both effective and balanced. The local response to lung infections includes neutrophil recruitment, expression of soluble mediators such as cytokines, and the extravasation of plasma constituents from the vascular space into the alveolar space. The result is an inflammatory milieu and cellular composition that promotes local immune responsiveness. This physiologic transition within the lung, however, occurs in tandem with a systemic acute phase response (APR), typified by altered circulating levels of acute phase proteins (APPs). While the APR has long been recognized as a useful biomarker of disease progression during pneumonia, the collective impact of APPs on inflammation and host defense are unknown. We have previously shown that the cytokines TNF-alpha, IL-1, and IL-6, which are critical for maximal host defense during pneumonia, are also essential for the activation of downstream transcription factors and the expression of APPs in the liver. Therefore, the hepatic APR may be a systemic conduit through which select cytokines promote the immune response to lung infection. Understanding how APPs and other extra-pulmonary factors integrate with local responses in the lung to promote immunity and tissue protection during pneumonia will help to identify novel prognostic indicators and therapeutics for this important disease.

In addition to the acute phase response, our laboratory is also interested in local factors controlling innate immunity and inflammation within the airspaces of infected lungs.  We have previously shown that signaling downstream of the transcription factor STAT3 is essential for tissue protection during pneumonia.  We are now particularly interested in the degree to which leukemia inhibitory factor (LIF), a STAT3-signaling cytokine, is responsible for calibrating acute pulmonary inflammation during pneumonia.

Selected Publications (since 2007):

  1. Yamamoto K, Ferrari JD, Cao Y, Ramirez MI, Jones MR, Quinton LJ, and Mizgerd JP (2012) Type I alveolar epithelial cells mount innate immune responses during pneumococcal pneumonia. Journal of Immunology (Epub ahead of print)
  2. Quinton LJ (corresponding author), Mizgerd JP, Hilliard KL, Jones MR, Kwon CY, and Allen E (2012) Leukemia inhibitory factor signaling is required for lung protection during pneumonia. Journal of Immunology 188 (12): 6300-8
    F1000 Article
  3. Quinton LJ (co-corresponding author), Blahna MT, Jones MR, Allen E, Hilliard KL, Ferrari JD, Zhang X, Sabharwal V, Algul H, Akira S, Schmid RM, Pelton SI, Spira A, and Mizgerd JP (2012) Combined hepatocyte-specific targeting of NF-κB RelA and STAT3 abrogates the acute phase response in mice. Journal of Clinical Investigation 122 (5): 1758-63
    F1000 Article
  4. Quinton LJ (2012) GM-CSF: A double dose of protection during pneumonia. American Journal of Physiology: Lung Cellular and Molecular Biology 302 (5): L445-6
  5. Blahna MT, Jones MR, Quinton LJ, Matsuura KY, and Mizgerd JP (2011) The terminal uridyltransferase enzyme zinc finger CCHC domain containing 11 (ZCCHC11) promotes cellular proliferation independent of its uridyltransferase activity. Journal of Biological Chemistry 286 (49): 42381-9
  6. Zamjahn J, Quinton LJ, Mack J, Frevert C, Nelson S, and Bagby GJ (2011) Differential flux of macrophage inflammatory protein-2 and cytokine-induced neutrophil chemoattractant from the lung after intrapulmonary delivery. American Journal of Physiology: Lung Cellular and Molecular Biology 301: L568-74
  7. Pittet LA, Quinton LJ, Yamamoto K, Robson BE, Ferrari JD, Algul H, Schmid RM, and Mizgerd JP (2011) Earliest innate immune responses require macrophage RelA during pneumococcal pneumonia. American Journal of Respiratory Cellular and Molecular Biology 45 (3): 573-81
  8. Quinton LJ and Mizgerd JP (2011) NF-KB and STAT3 signaling hubs for innate immunity. Cell and Tissue Research 343 (1): 153-65
  9. Jones MR, Quinton LJ, Blahna MT, Neilson JR, Fu S, Ivanov AR, Wolf DA, and Mizgerd JP (2009) Zcchc11-dependent uridylation of microRNA directs cytokine expression. Nature Cell Biology 11(9): 1157-63
  10. Quinton, L.J., Jones, M.R., Robson, B.E., and Mizgerd, J.P. (2009) Mechanisms of the hepatic acute phase response during bacterial pneumonia. Infection and Immunity 77: 2417-26
  11. Gamble, L., Bagby, G.J., Quinton, L.J., Happel, K.I., Mizgerd, J.P., Zhang, P., and Nelson, S. (2009) The systemic and pulmonary lipopolysaccharide binding protein response to intratracheal lipopolysaccharide. Shock 31 (2): 212-7
  12. Quinton, L.J., Jones, M.R., Robson, B.E., Simms, B.T., Whitsett, J.A., and Mizgerd, J.P. (2008) Alveolar epithelial STAT3, IL-6 family cytokines, and host defense during Escherichia coli pneumonia. American Journal of Respiratory Cell and Molecular Biology 38 (6): 699-706
  13. Happel, K.I., Rudner, X; Quinton, L.J., Movassaghi, J.L., Clark, C., Odden, A.R., Zhang, P., Bagby, G.J., Nelson, S., and Shellito, J.E. (2007) Acute alcohol intoxication suppresses the pulmonary ELR-negative CXC chemokine response to lipopolysaccharide. Alcohol 41 (5): 325-333
  14. Quinton, L.J., Jones, M.R., Simms, B.T., Kogan, M.S., Robson, B.E., Wilson, C.B., Skerrett, S.J., and Mizgerd, J.P. (2007) Functions and regulation of NF-kB RelA during pneumococcal pneumonia. Journal of Immunology 178 (3):1896-903.
  15. Johnston R.A., Mizgerd J.P., Flynt L., Quinton L.J., Williams E.S., and Shore S.A. (2007) Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in mice. American Journal of Respiratory Cell and Molecular Biology 37(4):477-484

Selected Reprints:

  1. Mechanisms of the hepatic acute phase response during bacterial pneumonia
  2. Alveolar epithelial STAT3, IL-6 family cytokines, and host defense during Escherichia coli pneumonia
  3. Functions and regulation of NF-kB RelA during pneumococcal pneumonia

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