Carol Wells, Ph.D.

Professor
612-625-5951
wells002@umn.edu

Research Interests

In vivo and in vitro interactions of microbes with intestinal epithelial cells.

Dr. Wells is a microbiologist who studies the process by which specific members of the normal intestinal microflora (e.g., Escherichia coli, Proteus mirabilis, Enterococcus faecalis, Candida albicans, C. glabrata) adhere to and penetrate the intestinal epithelial barrier. These translocating intestinal microbes are major causes of complicating infections in hospitalized immunosuppressed patients, postsurgical patients, and trauma patients. Researchers are finding that these microbes can interact with the intestinal epithelium and trigger a cascade of events that allows the organisms to enter other tissues, leading to systemic infection. But the routes and mechanisms of microbial transport have remained elusive due to the complex dynamics of the intestinal tract.

Wells and her colleagues are doing in vitro studies of microbial interactions (adherence, uptake, intracellular survival) with cultured intestinal epithelial cells. Data from in vitro studies are correlated with data from clinically relevant mouse models. Assay techniques include quantitative microbiological methods and light, immunofluorescent, and electron microscopic methods which enable the investigators to visualize microbial interactions with the intestinal epithelial barrier. The roles of several molecules relevant to intestinal epithelium are currently receiving particular emphasis, such as heparan sulfate proteoglycans (specifically syndecan-1).

Together, the mouse and cell culture experiments in Wells' laboratory have helped clarify the role of the intestinal epithelial cell in the process of microbial movement across the intestinal epithelium. Microbial transport across the intestinal mucosa appears to be a normal, low-level activity but can be stimulated to accelerate, particularly by trauma. These and additional findings of microbial virulence mechanisms may lead to the development of new treatment regimens that would decrease the costly morbidity associated with systemic infections caused by normal enteric flora.

Selected Recent Publications

• Feltis BA, Wells CL. Microbial translocation. Does it play a role in critical illness? Curr Opin Crit Care. 2000; 6:117-122.
• Wiesner, SM, Bendel CM, Hess DJ, Erlandsen SL, Wells CL. Adherence of yeast and filamentous forms of Candida albicans to cultured enterocytes.  Crit Care Med 2002;30:677-83.
• Bendel CM, Wiesner SM, Garni RM, Cebelinski E, Wells CL. Cecal colonization and systemic spread of Candida albicans in mice treated with antibiotics and dexamethasone. Pediatric Res. 2002; 51:290-5.
• Bendel CM, Hess DJ, Garni RM, Henry-Stanley M, Wells CL. Comparative virulence of Candida albicans yeast and filamentous forms in orally and intravenously inoculated mice.  Crit Care Med 2003;31:501-7.
• Kim AS, Garni RM, Henry-Stanley MJ, Bendel CM, Erlandsen SL, Wells CL. Hypoxia and extraintestinal dissemination of Candida albicans yeast forms.  Shock 2003;19:257-62.
• Henry-Stanley MJ, Hess DJ, Erickson EA, Garni RM, Wells CL. Role of heparan sulfate in interactions of Listeria monocytogenes with enterocytes.  Med Microbiol Immunol 2003;192:107-15.
• Hess DJ, Henry-Stanley MJ, Erickson EA, Garni RM, Wells CL. Intracellular survival of Staphylococcus aureus within cultured enterocytes. J Surg Res 2003; 114:42-49.
• Henry-Stanley MJ, Hess DJ, Erickson EA, Garni RM, Wells CL. Effect of lipopolysaccharide on virulence of intestinal Candida albicans.  J Surg Res 2003;113:42-49.
• Waters CM, Wells CL, Dunny GM. The aggregation domain of aggregation substance, not the RGD motifs, is critical for efficient HT-29 internalization.  Infect Immun 2003; 71:5682-5689.
• Erlandsen E, Chen Y, Frethem C, Detry J, Wells C. high resolution backscatter electron imaging of colloidal gold in LVSEM.  J Microscopy 2003; 211:212-218.