Jerry Nick, MD is Associate Professor of Medicine in the Pulmonary Division. He is Director of the Colorado Adult Cystic Fibrosis Program. He graduated from the University of Washington School of Medicine in 1989, and completed a Residency in Internal Medicine in 1992, also at the University of Washington. Following a Pulmonary and Critical Care Fellowship at the University of Colorado he joined the National Jewish Faculty in 1997.
The principal basic science interest of the group is the regulation of neutrophil response via intracellular signaling pathways. Much of this work has focused on the MAP Kinase cascades, and the response of neutrophils to LPS in the context of acute lung injury (ALI) and ARDS. More recently, we have examined these signaling mechanisms in the context of variability in neutrophil response, using a functional genomics approach. We are also very interested in better defining the response of the neutrophil to P. aeruginosa, as this is a principal event in CF lung disease.
Work relating to the response of neutrophil to P. aeruginosa has also led to an interest in the response of P. aeruginosa to neutrophils. Specifically, we have found that in the setting of excessive neutrophil death and necrosis, the bacteria is able to utilize neutrophil-derived DNA and F-actin as a scaffolding to accelerate the formation of biofilms. The biofilm phenotype evokes a tremendous survival advantage to P. aeruginosa, and represents a focus for therapeutic intervention in the prevention of and treatment of CF lung disease.
Integrated with basic studies of heterogeneity in neutrophil response are investigations of the variability of neutrophil response in the context of severity of disease in ARDS patients. This translational work seeks to correlate upregulation of interferon-stimulated genes with increased mortality in ARDS patients enrolled in ongoing ARDSNet trials.
The lack of sensitive and reliable markers of inflammation in CF lung disease is a major limitation in both patient care and the development of new therapies for the disease. We are conducting ongoing trials to validate the use of circulating monocyte RNA, as well as RNA derived from whole-blood, as a new biomarker for response to anti-inflammatory treatment in CF.
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