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CX3CL1 is involved in the ocular surface inflammation induced by benzalkonium chloride
Author(s) -
DENOYER A,
GODEFROY D,
FRUGIER J,
BAUDOUIN F,
ROSTèNE W,
BAUDOUIN C
Publication year - 2010
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2010.4455.x
Subject(s) - cx3cr1 , cxcr3 , benzalkonium chloride , chemokine , flow cytometry , cx3cl1 , inflammation , conjunctiva , immunology , chemotaxis , cell migration , chemokine receptor , receptor , biology , chemistry , cell , microbiology and biotechnology , pathology , medicine , biochemistry
Purpose To investigate whether the chemokine CX3CL1 could play a role in the conjunctival inflammatory cell trafficking induced by an exposure to benzalkonium chloride (BAC). Methods Expression of CX3CL1 was assessed in BAC‐exposed human conjunctival cell (HCC)line using flow cytometry and RT‐PCR. In vitro migration of leukocytes to BAC‐stimulated HCCs was assessed by migration assays and immuno flow cytometry with or without inhibition of CX3CR1. In vivo inflammatory cell trafficking was investigated by immunohistochemistry and confocal microscopy in the conjunctiva of wild‐type or CX3CR1‐deficient mice exposed to BAC. Results BAC induced an overexpression of CX3CL1 in HCCs. Leukocyte chemotaxis was observed when HCCs are stimulated with BAC. Human monocytic cells (CD45+,CD14+) and NK cells (CD45+,CD56+) migration was inhibited by blocking the CXCR3 receptor. In a mouse model of BAC‐induced ocular surface toxicity, the inflammatory cell infiltration of the conjunctiva was altered in the CX3CR1‐deficient mice compared to wild‐type. Conclusion The CX3CL1/CX3CR1 axis is involved in the BAC‐induced conjunctival inflammation. Specific blockade of this receptor could regulate the cell trafficking in the ocular surface.