Stephen T. Ballard, Ph.D.

Professor

 

Department of Physiology,
University of South Alabama
College of Medicine
MSB 3024
Mobile, AL 36688
Email: sballard@usamail.usouthal.edu

 

 

 

 

 

 


 

Ph.D., University of North Carolina
Postdoctoral Studies: Texas A&M University

Research Interests:

Control of the volume of surface liquid which covers the pulmonary epithelium is critical for normal mucociliary clearance and for efficient gas exchange. The role that active transepithelial ion transport plays as a driving force for liquid movement across the pulmonary airways is currently under study. We measure the bioelectric properties of isolated bronchi and bronchioles as correlates of active ion transport activity. We then use selective transport inhibitors and stimulators to determine which transport pathways are present and how these processes are regulated. In persons afflicted with cystic fibrosis (CF), a molecular defect in an epithelial chloride channel is present that leads to a myriad of pathological problems, the most critical of which involves secretion of thickened, dehydrated mucus into the airways. A major focus of our research is to determine how such defects in chloride ion transport are mechanistically related to the development of the symptoms observed in cystic fibrosis patients. Our findings suggest that fluid secretion from the submucosal glands of the trachea and bronchial airways is disrupted in CF, leading to the production of a highly concentrated mucus that is poorly cleared from the airways by cough or by mucociliary transport. We use techniques for measuring liquid secretion, mucociliary transport, and ciliary beat frequency to determine the importance of interactions between periciliary fluid, mucus, and cilia at the airway surface for maintaining normal ciliary clearance. We also model important aspects of CF lung disease in porcine isolated lungs by perfusing the vasculature with selective inhibitors of anion secretion. We are now expanding our studies by exploring new ways to model CF lung disease including  use of  in vitro (siRNA) and in vivo (screening non-humam animal populations for mutant CFTR) approaches. We believe that our findings are of great importance for understanding the underlying cause of CF lung disease and for development of effective treatments.

If you would like to know more about my work, or if you are interested in graduate or post-graduate studies in my laboratory, please feel free to e-mail me at sballard@usouthal.edu.  

        Selected Publications:

Ballard, S.T., J.D. Fountain, S.K. Inglis, and A.E. Taylor. Chloride secretion across distal airway epithelium: relationship to submucosal gland distribution. Am. J. Physiol. 268:L526-L531, 1995.

Corboz, M.R., S.T. Ballard, S.K. Inglis, and A.E. Taylor. Tracheal microvascular responses to inhibition of nitric oxide synthesis in anesthetized rats. Am. J. Respir. Crit Care Med. 154:1382-1386, 1996.

Corboz, M.R., S.T. Ballard, S.K. Inglis, and A.E. Taylor. Beta-adrenergic stimulation of the tracheal microvasculature in anesthetized rats. Am. J. Respir. Crit. Care Med. 153:1093, 1996.

Inglis, K.I., M.R. Corboz, A.E. Taylor, and S.T. Ballard. Regulation of ion transport across porcine distal bronchi. Am. J. Physiol. 14:L279-L297, 1996.

Corboz, M.R., S.T. Ballard, S.K. Inglis, and A.E. Taylor. Dilatory effect of furosemide on tracheal arterioles and venules. Am. J. Respir. Crit Care Med. 156:478-483, 1997.

Inglis, S.K., M.R. Corboz, A.E. Taylor, and S.T. Ballard. Effect of anion transport inhibition on mucus secretion by airway submucosal glands. Am. J. Physiol. 272:L372-L377, 1997.

Inglis, S.K., M.R. Corboz, A.E. Taylor, and S.T. Ballard. In situ visualization of bronchial submucosal glands and their secretory response to acetylcholine. Am. J. Physiol. 272:L203-L210, 1997.

Corboz, M.R., and S.T. Ballard. "Intravital microscopy: airway circulation," in Methods in Pulmonary Research, eds. S. Uhlig and A.E. Taylor, Birkauser-Verlag, Basel, 1998.

Inglis, S.K., M.R. Corboz, and S.T. Ballard. Effect of anion secretion inhibitors on mucin content of airway submucosal gland ducts. Am J. Physiol. 274:L762-L766, 1998.

Trout, L., M. King, W. Feng, S.K. Inglis, and S.T. Ballard. Inhibition of airway liquid secretion and its effects on the physical properties of airway mucus. Am. J. Physiol. 274:L258-L263, 1998.

Trout, L., J.T. Gatzy, and S.T. Ballard. Contribution of chloride and bicarbonate transport to acetylcholine-induced liquid secretion in porcine bronchial epithelium. Am. J. Physiol. 275:L1095-L1099, 1998.

Ballard, S.T., L. Trout, Z. Bebok, E.J. Sorscher, and A. Crews. CFTR involvement in chloride, bicarbonate and liquid secretion by airway submucosal glands. Am. J. Physiol. 277:L694-L699, 1999.

Corboz, M.R., S.T. Ballard, H. Gao, J.N. Benoit, S.K. Inglis, and A.E. Taylor. Differential effects of furosemide on porcine vascular and bronchial smooth muscle. J. Appl. Physiol. 89:1360-1364, 2000. 

Crews, A., A.E. Taylor, and S.T. Ballard. Liquid transport properties of tracheal epithelium. J. Appl. Physiol.91:797-802, 2001.

Trout, L., M.R. Corboz, and S.T. Ballard.  Mechanism of substance P-induced liquid secretion across porcine bronchial epithelium.  Am. J. Physiol. 281:L639-L645, 2001.

Ballard, S.T., L. Trout, A. Mehta, and S.K. Inglis.  Liquid secretion inhibitors reduce mucociliary transport in glandular airways.  Am. J. Physiol. 283:L329-L335, 2002.

Trout, L., M.I. Townsley, A. Bowden, and S.T. Ballard.  Disruptive effects of anion secretion inhibitors on airway mucus morphology in isolated perfused pig lungs.  J. Physiol. 549.3:845-853, 2003.

Ballard, S.T. and S.K. Inglis.  Liquid secretion properties of airway submucosal glands.  J. Physiol. 556.1:1-10, 2004.

Ballard, S.T.  Airway liquid secretion and cystic fibrosis lung disease.  News in Physiology  54:22-23, 2004.

Ballard, S.T., L. Trout, S.K. Inglis, and J. Garrison.  Ionic mechanism of forskolin-induced liquid secretion by porcine bronchi.  (in review)

Ballard S.T., J.C. Parker, and C.R. Hamm.  Restoration of mucociliary transport in the fluid-deplete trachea by surface-active substances.  (in review)