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Y. Ikeda, O. Masaharu, T. Flynn, M. Toda, S. Jerremy Ono; CCR1-Indpendent Allergic Conjunctivitis in a Murine Model. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2299.
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We have found that the macrophage inflammatory protein-1a (MIP1a) is a co-stimulatory factor for IgE-mediated mast cell degranulation in allergic conjunctivitis. Immediate hypersensitivity reactions in the conjunctiva were prevented in MIP1a deficient mice, in spite of normal numbers of tissue mast cells. MIP1a transcripts are rapidly induced after allergen exposure. Neutralizing antibodies with specificity for MIP1a also inhibited hypersensitivity in the conjunctiva. Moreover, the injection of MIP1a induces the rapid recruitment of neutrophils and eosinophils. CCR1 and CCR5 are CC chemokine receptors which can bind MIP1a. CCR1 is expressed on the surface of conjunctival mast cells, neutrophils and eosinophils. We do not detect CCR5 expression on conjunctival mast cells. We therefore postulate that the interaction with CCR1 on the conjunctival mast cell is pivotal in allergic conjunctivitis.
CCR1-deficient mice (C57BL/6 background) were sensitized and challenged with short ragweed pollen. The number of degranulated mast cell and eosinophils in the conjunctival tissues were calculated.
Clinical symptoms of CCR1-KO mice were remarkably similar to wild type mice. The mast cell degranulation ratio was more than 70% which was similar to that of wild type mice after conjunctuval allergen challenge. In addition, eosinophils influx in CCR1-KO mice was more pronounced than in wild type mice.
These data indicate that mice lacking CCR1 may develop ocular allergy via a distinct mechanism from wild-type mice. As mice lacking chemokine receptors are well documented to compensate by expression of other receptors, we hypothesize that CCR1-deficient mice may express CCR5 on conjunctival mast cells. We will present an analysis of the mast cell phenotype of CCR1-deficient mice.
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