Prenatal Exposure to Nicotine and Childhood Asthma: Role of Nicotine Acetylcholine Receptors, Neuropeptides, and Fibronectin Expression in Lung
Abstract
We hypothesize that prenatal exposure to nicotine, a major component of tobacco that transverses the placenta, is largely responsible for the development of asthma in children born of mothers who smoke. Specifically, we hypothesize that nicotine is recognized by specific cellular proteins called nicotinic acetylcholine receptors (nAChRs) that are expressed by lung cells termed fibroblasts and pulmonary neuroendocrine cells (PNEC). In fibroblasts, this interaction triggers the exaggerated expression of a connective tissue protein called fibronectin. In PNECs, nicotine stimulates cell growth and the excessive secretion of neuropeptides that affect airway formation and lung growth, and that stimulate smooth muscle cells to contract. In this fashion, nicotine can affect airways development and promote disease during childhood. This proposal will test the hypothesis in animal models of lung development and hyperreactive airways.
Document Details
- Document Type
- Technical Report
- Publication Date
- Dec 01, 2005
- Accession Number
- ADA452269
Entities
People
- Jesse Roman
Organizations
- Emory University