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My laboratory is interested in the study of the immune response to various
environmental insults (including respiratory viral infections, diesel particle
exposure, and allergen exposure) in neonates and their link to the development
of adult airway inflammation, asthma.
The occurrence of inflammatory respiratory diseases, such as asthma, has increased
dramatically in the past decade approaching epidemic levels among the peoples
of industrialized countries. Although a genetic basis for this disease state
has been suggested, environmental factors are partly responsible for the rising
trend. A major step forward in our understanding of asthma will occur when more
is known about the gene-environmental interactions and how they manifest into
airway disease. An ever-increasing number of studies have begun to suggest that
early exposure to various environmental insults orchestrate many of the events
critical to the development of asthma. The objective of my laboratory is to
realize the initiators of the immune and pathophysiological changes that occur
during the early stages of pulmonary airways disease and ultimately to understand
the fundamental causes of asthma so that more effective interventions and therapy
might be developed.
Our immediate goal is to determine if exposure during early neonatal life to environmental factors leads to predisposition, development of, or exacerbation of allergic respiratory disease in the adult. In the short term, we are exploring the validity of this hypothesis by accomplishing the following: (1) determining if respiratory viral infections initiate immune changes in the pulmonary microenvironment that predispose adults to pathologic responses to aeroallergens and (2) defining the molecular events initiated in response to allergen and viral insults. We believe these studies will offer intriguing new insights that will be relevant to the pathogenesis of human disease and could lead to novel interventions and/or therapy for the prevention of asthma.
Preliminary data in the laboratory demonstrated constitutive expression of
several eosinophil associated ribonucleases (Ears) in the lung and the
differential de novo expression of one of these Ears, Ear11, upon allergen challenge
or respiratory syncytial virus (RSV) infection. The mutual activation of Ear11
by RSV and allergen suggests that Ear11 lies downstream of both processes, supporting
hypotheses linking asthma immune responses and RSV infections - either as a
predisposing factor or as trigger. The mechanisms involved in virus-induced
asthma or asthma exacerbations are incompletely understood; however, our definition
of the gene regulatory mechanism(s) controlling Ear11 expression will represent
initial steps to resolve issues related to respiratory virus-induced pathologies.
1. Cormier SA, Taranova AG, Bedient C, Nguyen T, Protheroe
P, Pero R, Dimina D, Lenkiewicz E, Ochkur SI, O'Neill K, Colbert D, Lombari
TR, McGarry MP, Lee JJ, and Lee NA.. Eosinophil Infiltration of Solid Tumors
Is an Early Host Response That Potentially Modulates Cancer Growth. In press:
Journal of Leukocyte Biology.
2. Cormier SA, Backes WL, and Dellinger B. Health Impacts of
Toxic Combustion By-Products. Review. In Press: Environmental Health
Perspectives.
3. Becnel D,You D, Erskin J, Dimina DM, and Cormier SA. 2005.
A role for airway remodeling during respiratory syncytial virus infection. Respiratory
Research 6:122. Highly Accessed.
4. Lee JJ, Dimina DD, Macias MP, Ochkur SI, McGarry MP, O'Neill KR, Protheroe
C, Pero R, Nguyen T, Cormier SA, Lenkiewicz E, Colbert D, Rinaldi
L, Ackerman SJ, Irvin CG, and Lee NA. 2004. Mice Congenitally Deficient of Eosinophils
Define a Link with Asthma. Science. 305:1773-1776.[1]
5. Hao M, Cormier S, Wang M, Lee JJ, and Nel A. 2003. Diesel
Exhaust Particles Exert Acute Effects on Airway Inflammation and Function in
Murine Allergen Provocation Models. Journal of Allergy and Clinical Immunology.
1125:905-914.
6. Borchers MT, Biechele T, Justice P, Ansay T, Cormier S,
Mancino V, Wilkie TM, Simon MI, Lee NA and Lee JJ. 2003. Methacholine-induced
airway hyperresponsiveness is dependent on Gaq signaling. American Journal
of Physiology - LCMP. 285:L114-L120.
7. Shen H, Ochkur SI, McGarry MP, Crosby JR, Hines E M, Borchers MT, Wang H,
Biechele TL, O'Neill KR, Ansay TL, Colbert DC, Cormier SA,
Justice JP, Lee JJ, and Lee NA. 2003. A causative relationship exists between
eosinophils and the development of allergic pulmonary pathologies in the mouse.
Journal of Immunology. 170:3296-3305.
8. Cormier SA, Mello MA, and Kappen C. 2003. Normal proliferation
and differentiation of Hoxc-8 transgenic chondrocytes in vitro. BMC Dev
Biol 3(1):4.
9. Cormier S, Yuan S, Crosby J, Dimina D, Protheroe C, Lee
NA, and Lee JJ. 2002. TH2-mediated pulmonary inflammation leads to the differential
expression of ribonuclease genes by alveolar macrophages. American Journal
of Respiratory Cell and Molecular Biology. 27: 678-687.
10. Denzler KL, Borchers MT, Crosby JR, Cieslewicz G, Hines EM, Justice JP,
Cormier SA, Lindenberger KA, Song W, Wu W, Hazen SL, Gleich
GJ, Lee JJ, Lee NA. 2001. Extensive eosinophil degranulation and peroxidase-mediated
oxidation of airway proteins do not occur in a mouse ovalbumin-challenge model
of pulmonary inflammation. The Journal of Immunology. 167:1672-1682.
[1] Majority of work performed within Division of Pulmonary Medicine, Mayo Clinic
Scottsdale. Data was complied and written while at LSU.