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A. Denoyer, D. Godefroy, W. Rostène, C. Baudouin; Role of CX3CL1(Fractalkine) and CX3CR1 in the Trafficking of Inflammatory Cells in the Conjunctiva. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5531.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate whether CX3CL1 chemokine and its receptor CX3CR1 could influence cell interactions in conjunctival inflammatory processes.
Cultured human conjunctival cells (HCCs) were assessed for CX3CL1 expression by immunocytochemistry and immunoflow cytometry (IFC) after exposure to TNF- or benzalkonium chloride (BAC). Interactions between HCCs and primary culture of human leukocytes were investigated in migration assays, with and without CX3CL1 inhibitor. The phenotype of migrating cells was characterized by IFC. Inflammatory cell infiltration of the ocular surface (OS) was assessed using confocal microscopy in CX3CR1gfp+ transgenic mice.
HCCs constitutively expressed CX3CL1. Exposure to TNF- or BAC enhanced CX3CL1 expression. In vitro migration of leukocytes was mediated by the CX3CL1 expression of HCCs, and inhibited when blocking CX3CL1/CX3CR1 interaction. Phenotype of the migrating cells included CD4+, CD8+, CD14+ and CD16+ cells. Finally in vivo intraepithelial migration of lymphocytes and monocyte-derived CX3CR1gfp+ cells was found in the mouse OS after toxic stress induced by BAC.
Inflammatory mediator- and toxic-induced modulations of CX3CL1 expression in the conjunctiva suggest that CX3CL1/CX3CR1 interaction could regulate the immune cell trafficking and could be a new target in the treatment of OS inflammatory diseases.
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