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Reduced Leukocyte Migration, but Normal Rolling and Arrest, in Interleukin-8 Receptor Homologue Knockout Mice

From the Departments of ¹ Ophthalmology, ² Medicine, and ³ Cell and Developmental Biology, Casey Eye Institute, Oregon Health Sciences University, Portland, Oregon.

PURPOSE. To determine the role of the murine interleukin-8 receptor homologue (mIL-8Rh, neutrophil chemokine CXC receptor 2) in leukocyte migration using intravital microscopy in a standardized model of eye inflammation, endotoxin-induced uveitis (EIU).

METHODS. Two hundred fifty nanograms of E. coli endotoxin was injected into the vitreous of knockout mIL-8Rh^-/- (n = 7) mice or heterozygous littermate mIL-8Rh^+/- controls (n = 7). Intravital microscopic examination of iris microvasculature was performed at baseline and 6 and 24 hours after endotoxin injection. The numbers of rolling (cells/mm² endothelial surface/min), sticking (cells/mm² endothelial surface), and infiltrating cells (cells/mm² iris tissue) were evaluated by digital off-line quantification.

RESULTS. The number of infiltrating cells was significantly reduced in mIL-8Rh^-/- mice: 406 ± 77 cells/mm² at 6 hours and 242 ± 50 cells/mm² at 24 hours in mIL-8Rh^+/- mice versus 14 ± 4 cells/mm² at 6 hours and 38 ± 11 cells/mm² at 24 hours in mIL-8Rh^-/- mice (P < 0.001). In contrast, the absence of the IL-8 receptor homologue did not reduce rolling or sticking.

CONCLUSIONS. Iris rhodamine angiography allows precise quantification of leukocyte–endothelial dynamics in the absence of surgical trauma. IL-8 and its homologues are known to be potent signals for leukocyte migration. Although IL-8 has previously been implicated in cell adhesion, video imaging in vivo demonstrated that deletion of the IL-8 receptor homologue had minimal effect on rolling or arrest in this model of inflammation.

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