ArticleAmerican journal of ophthalmology2013
Why does the healthy cornea resist Pseudomonas aeruginosa infection?
Article in American journal of ophthalmology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 79 citations in OpenAlex.
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- Review
- Differentially Expressed Genes ofInfection and drug resistance · 2022Article
- Antimicrobial Peptide Expression at the Ocular Surface and Their Therapeutic Use in the Treatment of Microbial Keratitis.Frontiers in microbiology · 2022Review
- Human tear fluid modulates the Pseudomonas aeruginosa transcriptome to alter antibiotic susceptibility.The ocular surface · 2021Article
- The Role of Elastase in Corneal Epithelial Barrier Dysfunction Caused by Pseudomonas aeruginosa Exoproteins.Investigative ophthalmology & visual science · 2021Article
- Transcription Factor EepR Is Required forAntibiotics (Basel, Switzerland) · 2021Article
- Systemic diseases and the cornea.Experimental eye research · 2021Review
- Attenuation ofVirulence · 2020Article
- Antimicrobial Activity of Poly-epsilon-lysine Peptide Hydrogels Against Pseudomonas aeruginosa.Investigative ophthalmology & visual science · 2020Article
- Bacteriological profiles and drug susceptibility of Streptococcus isolated from conjunctival sac of healthy children.BMC pediatrics · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo provide our perspective on why the cornea is resistant to infection based on our research results with Pseudomonas (P) aeruginosa. We focus on our current understanding of the interplay between bacteria, tear fluid, and the corneal epithelium that determines health as the usual outcome, and propose a theoretical model for how contact lens wear might change those interactions to enable susceptibility to P aeruginosa infection.
methodsUse of "null-infection" in vivo models, cultured human corneal epithelial cells, contact lens-wearing animal models, and bacterial genetics help to elucidate mechanisms by which P aeruginosa survives at the ocular surface, adheres, and traverses multilayered corneal epithelia. These models also help elucidate the molecular mechanisms of corneal epithelial innate defense.
resultsTear fluid and the corneal epithelium combine to make a formidable defense against P aeruginosa infection of the cornea. Part of that defense involves the expression of antimicrobials such as β-defensins, the cathelicidin LL-37, cytokeratin-derived antimicrobial peptides, and RNase7. Immunomodulators such as SP-D and ST2 also contribute. Innate defenses of the cornea depend in part on MyD88, a key adaptor protein of TLR and IL-1R signaling, but the basal lamina represents the final barrier to bacterial penetration. Overcoming these defenses involves P aeruginosa adaptation, expression of the type III secretion system, proteases, and P aeruginosa biofilm formation on contact lenses.
conclusionAfter more than 2 decades of research focused on understanding how contact lens wear predisposes to P aeruginosa infection, our working hypothesis places blame for microbial keratitis on bacterial adaptation to ocular surface defenses, combined with changes to the biochemistry of the corneal surface caused by trapping bacteria and tear fluid against the cornea under the lens.
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