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Related Experiment Videos

Host-parasite interactions in Staphylococcus aureus keratitis.

Bradley D Jett1, Michael S Gilmore

  • 1Department of Biology, Oklahoma Baptist University, Shawnee, Oklahoma 73190, USA.

DNA and Cell Biology
|August 9, 2002
PubMed
Summary

Staphylococcus aureus invades human corneal cells primarily through fibronectin-binding proteins, not global regulatory genes. This invasion involves host cell actin polymerization and tyrosine kinase activity, offering potential therapeutic targets for bacterial keratitis.

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Area of Science:

  • Ophthalmology
  • Microbiology
  • Cell Biology

Background:

  • Ulcerative keratitis is a significant ocular infection, with Staphylococcus aureus causing approximately 25% of cases.
  • The specific virulence factors of S. aureus and host responses in keratitis remain largely undefined.

Purpose of the Study:

  • To investigate the host-parasite relationship between S. aureus and human corneal epithelial cells (HCECs) in vitro.
  • To identify the bacterial factors and host cell mechanisms involved in S. aureus invasion of the cornea.

Main Methods:

  • Utilized wild-type S. aureus and isogenic mutants (agr, sar, fnbAB) to assess binding and invasion of HCEC monolayers.
  • Investigated host cell involvement by pre-treating HCECs with inhibitory agents like colchicine, cytochalasin D, and genistein.

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Main Results:

  • S. aureus adhered to and was internalized by HCECs, with invasion being saturable.
  • Mutants lacking agr and sar regulators showed no significant difference in invasion compared to wild-type.
  • Mutations in fibronectin-binding proteins A and B (fnbAB) reduced S. aureus invasion by 99%.

Conclusions:

  • Fibronectin-binding proteins are key S. aureus adhesins mediating invasion of HCECs.
  • HCEC internalization of S. aureus involves active host cell mechanisms, including actin polymerization and tyrosine kinase activity.
  • Findings suggest potential therapeutic strategies targeting these interactions for S. aureus keratitis.