Associate Professor, Physiology

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Address: P.O. Box 245051
Tucson, AZ 85724
Phone: (520) 626-2105
E-Mail: sboitano@email.arizona.edu

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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

Olsen CE, Liguori AE, Zong Y, Lantz RC, Burgess JL, Boitano S. Aug 2008. Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells. Am J Physiol Lung Cell Mol Physiol, 295:L293-302

Omsland A, Miranda KM, Friedman RL, Boitano S. Jul 2008. Bordetella bronchiseptica responses to physiological reactive nitrogen and oxygen stresses. FEMS Microbiol Lett, 284:92-101

Caldwell PT, Thorne PA, Johnson PD, Boitano S, Runyan RB, Selmin O. Jul 2008. Trichloroethylene disrupts cardiac gene expression and calcium homeostasis in rat myocytes. Toxicol Sci, 104:135-43

Isakson BE Olsen CE Boitano S. Aug 2006. Laminin-332 alters connexin profile, dye coupling and intercellular Ca2+ waves in ciliated tracheal epithelial cells. Respir Res, 7:105