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Departments of Medicine and Ophthalmology, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106
Infiltration of neutrophils and eosinophils into the mammalian
cornea can result in loss of corneal clarity and severe visual
impairment. To identify mediators of granulocyte recruitment to the
corneal stroma, we determined the relative contribution of chemokine
receptors CXC chemokine receptor (CXCR)-2 (IL-8R homologue) and CCR1
using a murine model of ocular onchocerciasis (river blindness) in
which neutrophils and eosinophils migrate from peripheral vessels to
the central cornea. CXCR2-/- and CCR1-/-
mice were immunized s.c. and injected into the corneal stroma with Ags
from the parasitic helminth Onchocerca volvulus. We
found that production of macrophage-inflammatory protein (MIP)-2, KC,
and MIP-1
was localized to the corneal stroma, rather than to the
epithelium, which was consistent with the location of neutrophils in
the cornea. CCR1 deficiency did not inhibit neutrophil or eosinophil
infiltration to the cornea or development of corneal opacification. In
marked contrast, neutrophil recruitment to the corneas of
CXCR2-/- mice was significantly impaired
(p < 0.0001 compared with control, BALB/c mice)
with only occasional neutrophils detected in the central cornea.
Furthermore, CXCR2-/- mice developed only mild corneal
opacification compared with BALB/c mice. These differences were not due
to impaired KC and MIP-2 production in the corneal stroma of
CXCR2-/- mice, which was similar to BALB/c mice.
Furthermore, although MIP-1 production was lower in
CXCR2-/- mice than BALB/c mice, eosinophil recruitment to
the cornea was not impaired. These observations demonstrate the
critical role for CXCR2 expression in neutrophil infiltration to the
cornea and may indicate a target for immune intervention in
neutrophil-mediated corneal inflammation.
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