Scott Boitano Ph.D.

Associate Professor, Physiology

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Research Interests

We use unique primary tissue culture models of lung epithelial cells to study the cellular and tissue function of the lung epithelium. The conducting airway epithelium is an active cellular layer made up of a variety of cell types that is typified by ciliated airway epithelial cells that contribute to mucociliary clearance. The epithelial layer that lines the alveoli of the distal mammalian lung is made up of two distinct cell types, alveolar type I (AT1) and alveolar type II (AT2) cells. Physiological functions of AT1 cells include the primary site of gas exchange and of AT2 cells include the production of critical secretions that keep the lung from collapsing. Just as importantly, AT2 cells serve as "stem cells" that divide, migrate and differentiate to reform the AT1/AT2 epithelial layer following insult or injury. Also important to studies in our laboratory, lung epithelial cells provide innate immune function via a variety of events. These events include: the establishment of an epithelial "barrier;" the secretion of anti-microbial and inflammatory effector molecules; and direct interaction with non-epithelial cells (e.g. alveolar macrophages) to further immune function.
Our current studies include three foci: 1) Host/Pathogen Interactions in the Airway; 2) Intercellular Communication in the Airway Epithelium; and 3) Re-establishment of a Functional Airway Epithelium following insult or injury. In the host/pathogen interaction studies, we are using a ciliated cell culture model to better understand early events in airway infection by primary colonizing bacteria from the Bordetellae. This includes elucidation of bacteria and host proteins that contribute to ciliary binding and the innate host defenses activated by this early host/pathogen interaction. In the intercellular communication studies we are elucidating the molecular mechanisms that allow for second messenger signaling within and between airway epithelial cells in the conducting airway and in the alveoli. In the epithelial repair foci, we are studying the contributions of extracellular matrix molecules and neighboring cells to the re-establishment of a functional airway epithelium following large-scale wounding or local disruption by toxicants and/or toxins.

Selected Publications

Field JA, Luna-Velasco A, Boitano SA, Shadman F, Ratner BD, Barnes C, Sierra-Alvarez R. May 2011. Cytotoxicity and physicochemical properties of hafnium oxide nanoparticles. Chemosphere,2011 May 21;

Flynn AN, Tillu DV, Asiedu MN, Hoffman J, Vagner J, Price TJ, Boitano S. May 2011. The Protease-activated Receptor-2-specific Agonists 2-Aminothiazol-4-yl-LIGRL-NH2 and 6-Aminonicotinyl-LIGRL-NH2 Stimulate Multiple Signaling Pathways to Induce Physiological Responses in Vitro and in Vivo. J Biol Chem, 286:19076-88

Sherwood CL, Lantz RC, Burgess JL, Boitano S. May 2011. Arsenic alters ATP-dependent Ca²+ signaling in human airway epithelial cell wound response. Toxicol Sci, 121:191-206

Boitano S, Flynn AN, Sherwood CL, Schulz SM, Hoffman J, Gruzinova I, Daines MO. Apr 2011. Alternaria alternata serine proteases induce lung inflammation and airway epithelial cell activation via PAR2. Am J Physiol Lung Cell Mol Physiol, 300:L605-14