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Published on: November 22, 2024

Innate immune regulation of Serratia marcescens-induced corneal inflammation and infection

Rong Zhou1, Rui Zhang, Yan Sun

  • 1Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, Ohio 44106, USA.

Investigative Ophthalmology & Visual Science
|October 4, 2012
PubMed
Abstract

Insights

Serratia marcescens infection triggers corneal inflammation via toll-like receptor 4 (TLR4) and interleukin-1 receptor type 1 (IL-1R1) pathways. Inhibiting these pathways may treat contact lens-related keratitis.

Area of Science:

  • Ophthalmology
  • Immunology
  • Microbiology

Background:

  • Serratia marcescens is a common cause of contact lens-associated keratitis.
  • Toll-like receptors (TLRs) and IL-1R1 play crucial roles in ocular immune responses.

Purpose of the Study:

  • To investigate the involvement of TLRs and IL-1R1 in S. marcescens-induced corneal inflammation and infection.
  • To elucidate the specific TLR pathways mediating the host response to S. marcescens in the cornea.

Main Methods:

  • Murine corneal abrasion model with S. marcescens inoculation and contact lens wear.
  • Confocal microscopy for inflammation assessment and neutrophil enumeration.
  • Bacterial quantification using colony-forming units (CFUs).

Main Results:

  • S. marcescens induced significant neutrophil infiltration, corneal thickening, and haze in wild-type mice.
  • Mice deficient in MyD88, IL-1R1, TLR4, or TLR4/5 exhibited impaired bacterial clearance.
  • TLR4/MD-2 pathway activation, even with heat-killed bacteria, was crucial for inflammation.

Conclusions:

  • S. marcescens triggers corneal inflammation through TLR4/MD-2/MyD88 and IL-1R1/MyD88 signaling pathways.
  • These pathways represent potential therapeutic targets for managing S. marcescens-induced keratitis.

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