Dr. Scott M. Drouin
- Regulation of airway epithelial cells by mediators of the innate immune system
- Complement system
- Cell biology
- Molecular biology
The research in this laboratory has focused on ascertaining the role of the complement system in local airway responses during inflammatory diseases such as asthma and assessing the impact of complement activation on airway epithelial cell function. Airway epithelial cells contribute much to the pathology of asthma by excessive secretion of mucus which leads to airway obstruction and production of chemokines which recruit inflammatory leukocytes into the lung. Since complement activation has been shown to contribute overall to the pathology in asthma in rodent models of allergic pulmonary inflammation, specific attention will be given to the ability of complement to regulate airway epithelial-associated functions which lead to airway obstruction by utilizing established techniques for culturing and differentiating primary airway epithelial cells isolated from mice deficient in components and receptors of the complement system.
Depending on the student’s interests, a tutorial in this laboratory would provide experience with lung physiology, immunology, animal models of lung disease, gene expression, cell signaling, and cell culture methodologies.
Drouin SM, Corry DB, Kildsgaard J, Hollman TJ, Wetsel RA (2002) Absence of the Complement anaphylatoxin C3a receptor suppresses Th2 effector functions in a murine model of pulmonary allergy. J. Immunol. 169: 5926-5933.
Drouin SM, Sinha M, Sfyroera G, Lambris JD, Wetsel RA (2006) A Protective Role for the Fifth Complement Component (C5) in Allergic Airway Disease. Am. J. Resp. Crit. Care Med. 173: 852-857.
Dillard P, Wetsel R, Drouin SM (2007) The Complement Anaphylatoxin C3a Regulates Muc5ac Expression by Airway Epithelial Clara Cells Independently of TH2 Responses. Am J Resp Crit Care Med. 175: 1250-1258.
Program in Immunology