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Departments of
*
Respiratory Medicine,
Allergy and Rheumatology, and
Bioregulatory Function, University of Tokyo Graduate School of Medicine, Tokyo, Japan;
§
Department of Pediatrics, National Mie Hospital, Mie, Japan; and
¶
Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan
We examined the expression of transcripts of a panel of chemokine
receptors in human eosinophils and found intense constitutive
expression of CXCR4 mRNA. Although surface CXCR4 protein was hardly
detectable in the peripheral blood or freshly isolated eosinophils,
surface expression of CXCR4 became gradually apparent during incubation
at 37°C. In contrast, the level of CCR3 expression was virtually
unchanged during the incubation. Stromal cell-derived factor-1
(SDF-1), the natural ligand of CXCR4, elicited an apparent
Ca2+ influx in these cells and induced a strong migratory
response comparable to that by eotaxin. The surface expression of CXCR4
in eosinophils was up-regulated by IFN-
, TNF-, and TGF-ß while
it was down-regulated by IL-4 and eosinophil-directed hemopoietins such
as IL-5. The CXCR4 expression did not always parallel the apoptotic
changes in cytokine-treated eosinophils. In contrast to IL-4 and
IFN-, IL-5 potently reduced the level of CXCR4 mRNA. It seems
unlikely that CXCR4 is fundamentally involved in the pathogenesis of
allergic disorders by inducing the migration of eosinophils toward
inflammatory sites, because a Th2-dominant state down-regulates
eosinophil CXCR4 expression. However, CXCR4 may affect the size of the
mobilizable pool by holding eosinophils at noninflamed tissues.
Th2-dominant state may favor the liberation of eosinophils by
down-regulating CXCR4 expression. The interplay between CXCR4 and
SDF-1 in eosinophils potentially plays an important role in the
accumulation of these cells at the allergic inflammatory
sites.
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