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R01EY034239 : Inflammasome-mediated corneal epithelial cell defenses inhibited by pathogenic bacteria
R01EY034239 : Inflammasome-mediated corneal epithelial cell defenses inhibited by pathogenic bacteria
PI: Abby Kroken
The healthy corneal surface is an effective barrier to bacteria, yet the bacterial pathogen Pseudomonas aeruginosa is able to infect the eye during contact lens wear. We discovered that corneal epithelial cells normally undergo pyroptosis, an inflammatory and lytic programmed cell death, in response to bacterial invasion; however, P. aeruginosa inhibits this host response with one of its toxins, Exotoxin S. We will investigate the importance of pyroptosis in resolving microbial encounters at the ocular surface, and also identify how P. aeruginosa is able to subvert this host defense mechanism.
Collaborators:
Student Grants and Fellowships
Student Grants and Fellowships
TLR2-mediated discrimination between pathogenic threats and non-threatening bacterial ligands in ocular surface cells
TLR2-mediated discrimination between pathogenic threats and non-threatening bacterial ligands in ocular surface cells
PI: Rachel Mazurek, PhD Candidate
Bacteria such as Pseudomonas aeruginosa (Pa) can cause an infection called infectious corneal keratitis that can lead to permanent vision loss or blindness. This occurs when Pa passes through corneal surface cells and deeper into the corneal tissue. The events leading up to and following a corneal keratitis infection are fairly well understood, however the early response and detection of Pa by corneal epithelial cells (CECs) remain understudied. It is, however, known that CECs play an active role in preventing corneal infections. This project will investigate how CECs detect and respond to Pa and how these responses protect from infection.
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