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1 From the Neurologic Sciences Institute, Oregon Health and Science University, Portland.
PURPOSE. To determine the pattern of expression of CC chemokines and their receptors in the eyes of Lewis rats and to establish their role in autoimmune anterior uveitis (AU) associated with experimental autoimmune encephalomyelitis (EAE).
METHODS. EAE/AU was induced in Lewis rats with myelin basic protein in complete
Freund’s adjuvant (CFA). The rats were scored for the development of
clinical EAE and AU. The expression of CCL5/regulated on
activation normal T-cell expressed and secreted (RANTES), CCL2/monocyte
chemotactic protein (MCP)-1, CCL3/macrophage inflammatory protein
(MIP)-1
, and CCL4/MIP-1ß and their receptors was examined at the
preclinical stage, onset, peak, and recovery by RT-PCR and ELISA.
EAE/AU rats were treated with neutralizing polyclonal antibodies
against CCL3/MIP-1, CCL4/MIP-1ß, CCL2/MCP-1, and CCL5/RANTES and
tested for the suppression of onset of clinical AU and EAE. The control
group received normal rabbit IgG at the same dose.
RESULTS. The gene expression of those chemokines was upregulated concurrently
with symptom onset of EAE/AU and correlated with the intensity of
inflammatory changes in the eye and central nervous system (CNS). The
highest expression of CCL4/RANTES, CCL2/MCP-1, and CCL3/MIP-1 in the
eye was detected at onset of clinical uveitis, whereas CCL4/MIP-1ß
was elevated at the peak of AU. The expression of chemokine receptors
associated with T-helper (Th)1-type response, CCR1 and CCR5, correlated
with their appropriate ligands and was the highest at the peak of AU,
whereas CCR2, the receptor for CCL2/MCP-1, was present before the onset
of the disease. Treatment of anti-MIP-1ß and anti-MCP-1 significantly
delayed the onset and shortened the duration of AU and EAE.
Anti-MIP-1 treatment had no effect on clinical EAE but inhibited the
clinical signs of AU. Although CCL5/RANTES expression was observed
during the entire course of the disease, anti-RANTES treatment had no
effect on clinical disease progression.
CONCLUSIONS. The data suggest that CCL2/MCP-1, CCL3/MIP-1, and CCL4/MIP-ß
contribute to the recruitment of inflammatory cells into the eye and
CNS and to disease activity.
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