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Signaling in Airway Inflammation
Project Summary:
Signaling in Airway Inflammation
1PO1 AI062885 (NIAID)
Project dates: 7/2005-4/2010
Principal Investigators:
- Allan Brasier, M.D.
- Roberto Garofalo, M.D.
- Antonella Casola, M.D.
- Sanjiv Sur, M.D.
- Istvan Boldogh, Ph.D.
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This is a prestigious National Institutes of Health (NIH)-funded program project grant to investigate the effect of specific intracellular signaling pathways initiated by reactive oxygen species (ROS), airway inflammation and asthma.
Asthma is a major public health problem that affects over 18 million Americans and causes billions of dollars in hospitalization costs and work absenteeism. In children, asthma is a leading cause of lost days at school. Asthma is a disease that affects the airways and is now recognized to be the result of tissue inflammation. The lining epithelial cells of the lung represents the first tissues that come into contact with inhaled viruses or pollens.
This PPG application is composed of 5 inter-related projects investigating the hypothesis that ROS initiated signaling is an important event early in the process of airway inflammation. Upon contact with Respiratory Syncytial Virus (RSV) or allergens, the epithelium is exposed to enhanced ROS tone. ROS initiates airway inflammation by activating intracellular signaling pathways through nuclear factor-kB (NF-kB) and
Signal Transducers and Activators of Transcription (STATs). These signaling molecules induce the expression and secretion of chemokines.
Chemokines, in turn, lead to leukocytic accumulation in the airway, and airway hyper-reactivity (asthma). Our studies will result in identification of novel targets that influence epithelial cell responses to common exacerbants of asthma.
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