April 2014
Volume 55, Issue 13
ARVO Annual Meeting Abstract  |   April 2014
Role of Chemokine C-C motif ligand 7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis
Author Affiliations & Notes
  • Chuan-Hui Kuo
    Allergy & Immunology, Cincinnati Children's Hospital, Cincinnati, OH
  • Andrea Collins
    Allergy & Immunology, Cincinnati Children's Hospital, Cincinnati, OH
  • Santa J Ono
    Allergy & Immunology, Cincinnati Children's Hospital, Cincinnati, OH
    University of Cincinnati, Cincinnati, OH
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 2486. doi:
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      Chuan-Hui Kuo, Andrea Collins, Santa J Ono; Role of Chemokine C-C motif ligand 7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis. Invest. Ophthalmol. Vis. Sci. 2014;55(13):2486.

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

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Purpose: Molecules that are necessary for ocular hypersensitivity reactions include the chemokine receptors CCR1 and CCR3; chemokine C-C motif ligand 7 (CCL7) is a genetic target and ligand for these receptors. Therefore, we hypothesized that CCL7 mediates ocular hypersensitivity reactions and investigated CCL7’s necessity in a murine model of IgE-mediated allergic conjunctivitis using wild-type (WT) and CCL7-deficient mice.

Methods: Allergic conjunctivitis was induced in WT and CCL7-deficient mice. Mice were sensitized with OVA/alum intraperitoneally and subjected to OVA-induced ocular anaphylaxis via eye drops. Early-phase reactions including clinical symptoms, gene expressions and pathological changes in the conjunctival tissue were evaluated. Bone marrow-derived mast cells (BMMCs) from WT and CCL7-deficient mice were sensitized and activated. β-hexosaminidase activity was measured by incubating the supernatants with p-nitrophenyl N-acetyl-β-D- glucosaminide.

Results: The early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized than in vehicle-sensitized WT mice, but this OVA-induced increase was suppressed in CCL7-deficient mice. The mRNAs for FcεRIα and the connective tissue-type mast cell proteases were detected in the conjunctiva of both OVA-induced WT and CCL7-deficient mice. Notably, in OVA-induced anaphylaxis, the number of conjunctival mast cells was lower in CCL7-deficient than in WT mice, and BMMCs from CCL7-deficient mice showed decreased degranulation with IgE and antigen treatment compared with BMMCs from WT mice.

Conclusions: Our results demonstrate that chemokine CCL7 deficiency suppressed OVA-induced ocular anaphylaxis, including regulating mast cell recruitment in vivo and reducing FcεRI-mediated mast cell activation in vitro. A better understanding of CCL7’s roles in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

Keywords: 475 conjunctivitis • 490 cytokines/chemokines  

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