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The effect of nicotine on airway inflammation

Institution: University of Southern California
Investigator(s): Omid Akbari, Ph.D.
Award Cycle: 2009 (Cycle 18) Grant #: 18XT-0160 Award: $402,991
Subject Area: Pulmonary Disease
Award Type: Exploratory/Developmental Award

Initial Award Abstract
Chronic Airway hyperreactivity (AHR), a cardinal feature of asthma and chronic obstructive pulmonary disease (COPD) affects more than 20 million individuals in the United States. Many Americans are affected by a serious chronic lung condition characterized by episodes or attacks of inflammation and narrowing of the small airways in response to certain triggering agents. The proposed project addresses many basic scientific questions that will help to understand the mechanisms resulting in airway sensitization and the development of lung inflammation. Our preliminary data suggest that one major trigger for lung diseases is exposure to nicotine, whether through active or second hand exposure to cigarette smoking. Since disruption of airway mucosal homeostasis is an important factor in the induction of airway sensitization, airway resident cells or their products may affect the outcome of exposure to triggers such as nicotine. It is therefore important to elucidate how immune cells located in airway mucosa could interact with each other and play a role in the development of AHR.

Today, many different treatments for lung diseases are available. However, they only help patients to breathe easier, and they also reduce the swelling and inflammation in the air tubes for a short period of time. But one way to prevent lung diseases, to reduce the incidence and exacerbation of lung disease and to discover cures for lung disease and improve it’s diagnosis and treatment is to strongly support research, and especially the understanding of the molecular and cellular mechanisms involved. We believe targeting bronchial immune cells, such as T cell subsets and Natural Killer T cells (NKT), which are directly present and responsible for lung inflammation and AHR, would be potentially a more direct, physiological and specific therapy than any other treatments. Since our preliminary results suggest that the number of lung NKT cells increase in lungs after exposure to nicotine, we intend to study the effect of nicotine on activation of NKT cells. We believe that exposure to smoke and nicotine might affect the number and activation mode of NKT cells in the lungs and therefore directly affect the development of airway inflammation and AHR. The results of our proposed studies might help to explain why active and second hand smoking is a risk factor for the onset of airway inflammation, such as COPD and asthma. A better understanding of the mechanisms resulting in airway sensitization is a valuable approach towards therapy and because of the possible clinical relevance by targeting cells that are responsible for lung inflammation, major progress is to be expected.