Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Contact lens wear reduces adhesion of commensal bacteria to superficially-injured murine corneas
Author Affiliations & Notes
  • David J Evans
    Herbert Wertheim School of Optometry & Vision Science, University of California Berkeley, Berkeley, California, United States
    College of Pharmacy, Touro University California, Vallejo, California, United States
  • Yujia Yang
    Herbert Wertheim School of Optometry & Vision Science, University of California Berkeley, Berkeley, California, United States
  • Orneika Flandrin
    Herbert Wertheim School of Optometry & Vision Science, University of California Berkeley, Berkeley, California, United States
  • Suzanne M J Fleiszig
    Herbert Wertheim School of Optometry & Vision Science, University of California Berkeley, Berkeley, California, United States
  • Footnotes
    Commercial Relationships   David Evans None; Yujia Yang None; Orneika Flandrin None; Suzanne Fleiszig None
  • Footnotes
    Support  EY030350
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 3297. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      David J Evans, Yujia Yang, Orneika Flandrin, Suzanne M J Fleiszig; Contact lens wear reduces adhesion of commensal bacteria to superficially-injured murine corneas. Invest. Ophthalmol. Vis. Sci. 2024;65(7):3297.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose : Previously we have shown that contact lens wear can induce corneal para-inflammation, involving several types of immune cells: e.g. CD11c+, Lyz2+ and γδ-T cells after 24 h of wear, γδ-T cells, Lyz2+ cells and Ly6G+ cells (neutrophils) after 6-7 days wear. Here, we tested the hypothesis that contact lens wear protects corneas against adhesion by commensal bacteria.

Methods : LysMcre mice were used to image corneal Lyz2+-GFP cells (myeloid-derived). One eye of each mouse was fitted with a custom-made contact lens (CL); contralateral eyes did not wear lenses (NCL). After 4-6 days lens wear, mice were anesthetized and corneas superficially-injured by tissue paper blot to promote bacterial adhesion. Eyes were inoculated with 5 μl of ~1011 CFU/mL Macrococcus spp. (a murine eyelid commensal) each hour for 4 h. Mice were euthanized and enucleated eyes fixed in 2% paraformaldehyde overnight and a universal bacterial 16S rRNA FISH probe used to label adherent bacteria. Confocal microscopy was used to quantify bacterial adhesion, epithelial traversal and Lyz2+ cells using Imaris software. Student’s t-test was used for statistical analysis. P < 0.05 was considered significant.

Results : Contact lens wear increased corneal Lyz2+ cell numbers compared to no lens wear: CL 58.6 ± 7.3 vs. NCL 36 ± 4.6 cells/field of view (mean ± SEM, P < 0.05). Moreover, more Lyz2+ cells were found within the corneal epithelium or extending processes into the epithelium: CL 3.7 ± 0.5 vs. NCL 1.6 ± 0.5 cells/field of view (P < 0.05). Lens-wearing corneas showed significantly fewer adherent bacteria than no lens wear: CL 175.7 ± 59.3 vs. NCL 454 ± 190.7 bacteria/field of view (P < 0.05). However, adherent bacteria traversed further into the epithelium with lens wear: CL 4.5 ± 0.5 vs NCL 2.2 ± 0.2 μm (P < 0.0001).

Conclusions : Contact lens wear induces corneal parainflammation and also protects superficially-injured corneas against adhesion of commensal bacteria. The role of lens-induced parainflammation in protecting against bacterial colonization remains to be determined, as does the significance of deeper epithelial penetration by colonizing bacteria in lens-wearing corneas.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×