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KC production in the cornea in response to Pseudomonas aeruginosa challenge
1Cooperative Research Centre for Eye Research and Technology, School of Optometry, University of New South Wales, Sydney, New South Wales, Australia.
Abstract:
Pseudomonas aeruginosa can cause ulcerative bacterial keratitis. A feature of keratitis is the rapid infiltration of the avascular corneal stroma by neutrophils. KC is a potent neutrophil chemokine. The present study used a mouse model of ocular infection to assess the relationship between KC and inflammation in the cornea in response to challenge with a strain of P. aeruginosa causing keratitis. Low levels of KC mRNA and protein were detected by in situ hybridization and ELISA, respectively, in unchallenged corneas. Dramatically increased numbers of KC mRNA+ cells were present in P. aeruginosa strain 6294-challenged corneas. Expression of KC mRNA was found to be up-regulated in the corneal epithelium in response to wounding alone. The KC mRNA+ cells were located in the epithelium and corresponding to infiltrating neutrophils cells in the stroma. Quantification of KC protein at different time points showed peak levels at 8 h of bacterial challenge. These results suggest that KC may be involved with the regulation of leucocyte infiltration early during bacterial keratitis.
Insights
Keratitis, an eye infection, involves neutrophil infiltration. This study found that KC, a chemokine, increases with Pseudomonas aeruginosa infection, suggesting its role in early inflammation and neutrophil recruitment to the cornea.
Area of Science:
- Ophthalmology
- Immunology
- Microbiology
Background:
- Pseudomonas aeruginosa is a common cause of bacterial keratitis.
- Neutrophil infiltration into the avascular cornea is a hallmark of keratitis.
- KC is a known neutrophil chemokine.
Purpose of the Study:
- To investigate the role of KC in corneal inflammation during P. aeruginosa-induced keratitis using a mouse model.
- To assess the relationship between KC expression and neutrophil infiltration in the cornea.
Main Methods:
- Mouse model of P. aeruginosa ocular infection.
- In situ hybridization to detect KC mRNA.
- ELISA to quantify KC protein levels.
- Corneal tissue analysis for KC mRNA+ cells and neutrophils.
Main Results:
- KC mRNA and protein levels were low in unchallenged corneas.
- P. aeruginosa challenge significantly increased KC mRNA+ cells in the cornea.
- KC mRNA expression was also upregulated in response to corneal wounding alone.
- Peak KC protein levels were observed at 8 hours post-infection.
- KC mRNA+ cells were found in the epithelium, correlating with neutrophil infiltration in the stroma.
Conclusions:
- KC expression is upregulated during P. aeruginosa keratitis.
- KC may play a significant role in regulating early leukocyte infiltration into the cornea during bacterial keratitis.