Lee Quinton, Ph.D.
Associate Professor of Medicine, Pathology and Microbiology
72 East Concord Street, R208
B.S. University of Southern Mississippi, Hattiesburg
Ph.D. Louisiana State University Health Sciences Center
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 elicit 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 leukocyte recruitment, elaboration of soluble mediators such as cytokines, and the extravasation of plasma constituents into the alveolar space, resulting in an inflammatory milieu 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 liver-derived 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 now identified pathways up- and down-stream of liver acute-phase activation, and we have developed genetic mouse models and cell culture systems to interrogate causal relationships between liver and lung responses. Understanding how this lung-liver axis coordinates pulmonary homeostasis during pneumonia will help to identify novel prognostic indicators and therapeutics for this important disease.
In addition to the lung-liver axis, our laboratory investigates locally-derived factors controlling innate immunity and tissue integrity within the airspaces of infected lungs. In particular, we are investigating signaling networks that help to maintain the resilience of lung epithelium, which is exquisitely vulnerable to damaging environmental and/or host factors present in the pneumonic lung. A more complete understanding of these pathways may pave the way for novel clinical interventions in patients with or at risk for pneumonia and acute lung injury.
- Quinton, L.J., Walkey, A.J., and Mizgerd, J.P. (2018) Integrative Physiology of Pneumonia. Physiological Reviews (in press)
- Quinton, L.J. and Mizgerd, J.M. (2015) Dynamics of lung defense in pneumonia: resistance, resilience, and remodeling. Annu Rev Physiol 77:407-30. PMID: 25148693
Original research articles:
- Traber, K.E., Symer, E.M., Allen, E., Kim, Y., Hilliard, K.L., Wasserman, G.A., Stewart, C.L., Jones, M.R., Mizgerd, J.P., and Quinton, L.J. (2017) Myeloid-epithelial crosstalk coordinates synthesis of the tissue protective cytokine leukemia inhibitory factor during pneumonia. Am J Physiol Lung Cell Mol Physiol 313:L548-L558. PMID: 28522567
- Hilliard, K.L., Allen, E., Traber, K.E., Kim, Y., Jones, M.R., Mizgerd, J.P., and Quinton, L.J. (2015) Activation of hepatic STAT3 maintains pulmonary defense during endotoxemia. Infect Immun 83(10): 4015-27. PMID: 26216424
- Traber, K.E., Allen, B.A., Hilliard, K.L., Yamamoto, K., Jones, M.R., Mizgerd, J.P., and Quinton, L.J. (2015) Oncostatin M is required for maximal CXCL5 expression and neutrophil recruitment during pneumonia. Am J Respir Cell Mol Biol 53(4): 479-88. PMID: 25692402
- Hilliard, K.L., Allen, E., Traber, K.E., Yamamoto, K., Stauffer, N.M., Wasserman, G.A., Jones, M.R., Mizgerd, J.P., and Quinton, L.J. (2015) The lung-liver axis facilitates pulmonary innate immunity and hepatoprotection during pneumonia. Amer J Respir Cell Mol Biol 53(3): 378-90. PMID: 25607543
- Quinton, L.J., Mizgerd, J.P., Hilliard, K.L., Jones, M.R., Kwon, C.Y., and Allen, E. (2012) Leukemia inhibitory factor signaling is required for lung protection during pneumonia. J Immunol 188(12): 6300-8. PMID: 22581855
- Quinton, L.J., Blahna, M.T., Jones, M.R., Allen, E., Hilliard, K.L., Ferrari, J.D., Zhang, X., Sabharwal, V., Algül, H., Akira, S., Schmid, R.M., Pelton, S.I., Spira, A., and Mizgerd, J.P. (2012) Hepatocyte-specific mutation of both NF-kB RelA and STAT3 abrogates the acute phase response in mice. J Clin Invest 122(5): 1758-63. PMID: 22466650
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