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Original article
The murine CCR3 receptor regulates both eosinophilia and hyperresponsiveness in IgE-mediated allergic conjunctivitis
  1. Ken Fukuda1,2,
  2. Chuan-Hui Kuo1,3,
  3. Kei Morohoshi1,4,
  4. Fu-Tong Liu5,
  5. Santa Jeremy Ono1,3,6
  1. 1Department of Ophthalmology, Emory University School of Medicine, Atlanta, Georgia, USA
  2. 2Department of Ophthalmology, Kochi Medical School, Kochi, Japan
  3. 3Department of Allergy and Immunology, Cincinnati Children's Hospital, Cincinnati, Ohio, USA
  4. 4Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, Tokyo, Japan
  5. 5Department of Dermatology, University of California Davis School of Medicine, Sacramento, California, USA
  6. 6University of Cincinnati, Cincinnati, Ohio, USA
  1. Correspondence to Dr Ken Fukuda, Department of Ophthalmology, Kochi Medical School, Oko-cho, Kohasu, Nankoku-city, Kochi 783-8505, Japan; k.fukuda{at}kochi-u.ac.jp

Abstract

Background/aims Allergic conjunctivitis is characterised by early-phase clinical symptoms and late-phase inflammation in the conjunctiva. The role of different chemokine receptors in allergic conjunctivitis, especially during the early-phase reaction, is still unclear. We investigated the importance of CC chemokine receptor (CCR) 3 in a murine model of IgE-mediated allergic conjunctivitis using CCR3-deficient (CCR3−/−) mice.

Methods Allergic conjunctivitis was initiated in wild-type (WT) and CCR3−/− mice by passive transfer of ragweed (RW)-specific IgE, followed by topical challenge with RW in eye drops. Early-phase reactions including clinical symptoms and vascular leakage, as well as late-phase eosinophil infiltration of the conjunctiva were evaluated. The expression of mRNAs in the conjunctiva was quantified by real-time PCR analysis.

Results The number of infiltrated eosinophils in the conjunctiva following RW challenge, was significantly higher in RW-IgE-sensitised WT mice compared with those sensitised with phosphate-buffered saline for WT, but this was not observed in similarly treated CCR3−/− mice. The early-phase clinical symptoms and vascular leakage were also suppressed in CCR3−/− mice. The number of conjunctival mast cells were not different between CCR3−/− mice and WT mice, and the mRNAs for FcɛRІα and the connective tissue-type mast cell proteases were detected in the conjunctiva of both WT and CCR3−/− mice. RW-IgE-sensitised CCR3−/− mice displayed significantly reduced expression of CCL2, CCL3, and IL-6 compared with WT mice.

Conclusions These results demonstrate a direct contribution of CCR3 to both the early-phase reaction and late-phase inflammation during ocular allergy.

  • Allergic conjunctivitis
  • mast cell
  • chemokine receptor
  • eosinophil
  • experimental and animal models
  • conjunctiva
  • inflammation
  • infection
  • experimental and laboratory
  • eye lids
  • immunology
  • ocular surface

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Footnotes

  • The present data have not been presented previously.

  • Funding This work was supported by NIH grant number R01-EY1901 (SO).

  • Competing interests None.

  • Patient consent It is an animal experiment.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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