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Pathogenic strains of Acanthamoeba are recognized by TLR4 and initiated inflammatory responses in the cornea

Hassan Alizadeh1, Trivendra Tripathi1, Mahshid Abdi1

  • 1Department of Cell Biology and Immunology, University of North Texas Health Science Center, and North Texas Eye Research Institute, Fort Worth, Texas, United States of America.

Plos One
|March 18, 2014
PubMed

Insights

Toll-like receptor 4 (TLR4) is activated by pathogenic Acanthamoeba, initiating inflammatory responses in the cornea. This suggests TLR4 is a potential therapeutic target for Acanthamoeba keratitis (AK).

Area of Science:

  • Ophthalmology
  • Immunology
  • Microbiology

Background:

  • Acanthamoeba keratitis (AK) is a severe corneal infection caused by Acanthamoeba species.
  • Innate immunity, particularly Toll-like receptors (TLRs), plays a crucial role in combating AK.

Purpose of the Study:

  • To investigate whether Acanthamoeba activates TLRs on corneal epithelial cells, triggering inflammatory responses.
  • To determine the specific role of TLR4 in the pathogenesis of AK.

Main Methods:

  • Human corneal epithelial (HCE) cells and HEK-293 cells expressing TLRs were stimulated with Acanthamoeba castellanii.
  • Gene and protein expression of inflammatory markers (IL-8, CXCL2) and TLRs were analyzed.
  • In vivo studies used a Chinese hamster model of AK, assessing TLR4 activation and CXCL2 production.

Main Results:

  • Acanthamoeba castellanii upregulated TLR4 and IL-8 in HCE cells.
  • TLR4 activation by Acanthamoeba led to IL-8 production in HEK-293 cells, which was inhibited by a TLR4 neutralizing antibody.
  • Clinical strains of Acanthamoeba activated TLR4 and induced CXCL2 production in vivo, correlating with inflammation.

Conclusions:

  • Pathogenic Acanthamoeba species activate TLR4, leading to inflammatory cytokine production.
  • TLR4 is implicated in the innate immune response to Acanthamoeba keratitis.
  • TLR4 represents a potential therapeutic target for AK and other microbial corneal infections.

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