Joy Sturtevant, PhD

Pathogens have evolved to thwart our immune response and/or 'peacefully' reside within our body. How do they  do  this?  Our  laboratory  focuses  on  the  initial  interactions  between  pathogen  and  host,  and  the intracellular  signaling  events  that  dictate  a  response  in  either  host  or  pathogen.  We  are  studying  two different  microorganisms  to  address  these  responses.  First,  we  are  studying  Candida  albicans,  the  most common opportunistic  fungal pathogen and the 4th most common nosocomial infectious agent but also a member of the normal microbiota. The ability of the pathogenic fungus Candida albicans to cause disease requires rapid adaptation to changes in the host environment and to an evolving host immune response. We are particularly  interested  in Candida  ‘survival’  factors and their effect on host-­‐pathogen  interaction.  The second project is a collaborative  venture with Dr. Haas in Biochemistry.  This project is researching on how Shigella  Type  III  secretion  proteins  reprogram  the  host  innate  immune  response.  Shigella  is  a  major contributor to gastroenteritis and the causative agent of dysentery. We are focusing on how Shigella E3 type ubiquitin ligases usurp host signaling pathways. We feel that these studies will advance our knowledge  of how  pathogens  adapt  and  survive  in  the  host  and  will  assist  in  the  identification  of  new  antimicrobial strategies.  Molecular  genetic,  proteomic,  cell  culture  and  cell  biology  techniques  are  used  to  answer  these questions.