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*
Laboratory of Molecular Immunoregulation,
Laboratory of Experimental Immunology, Division of Basic Sciences,
Intramural Research Support Program, Science Applications International Corp., and
Veterinary and Tumor Pathology Section, Office of Laboratory Animal Resources, Frederick Cancer Research and Development Center, Frederick, MD 21702; and
¶ Cell Biology Section, National Institute of Dental and Craniofacial Research, Bethesda, MD 20892
Chemokines are attractants and regulators of cell activation.
Several CXC family chemokine members induce angiogenesis and promote
tumor growth. In contrast, the only CC chemokine, reported to play a
direct role in angiogenesis is monocyte-chemotactic protein-1. Here we
report that another CC chemokine, eotaxin (also known as CCL11), also
induced chemotaxis of human microvascular endothelial cells.
CCL11-induced chemotactic responses were comparable with those induced
by monocyte-chemotactic protein-1 (CCL2), but lower than those induced
by stroma-derived factor-1
(CXCL12) and IL-8 (CXCL8). The
chemotactic activity was consistent with the expression of CCR3, the
receptor for CCL11, on human microvascular endothelial cells and was
inhibited by mAbs to either human CCL11 or human CCR3. CCL11 also
induced the formation of blood vessels in vivo as assessed by the chick
chorioallantoic membrane and Matrigel plug assays. The angiogenic
response induced by CCL11 was about one-half of that induced by basic
fibroblast factor, and it was accompanied by an inflammatory
infiltrate, which consisted predominantly of eosinophils. Because the
rat aortic sprouting assay, which is not infiltrated by eosinophils,
yielded a positive response to CCL11, this angiogenic response appears
to be direct and is not mediated by eosinophil products. This suggests
that CCL11 may contribute to angiogenesis in conditions characterized
by increased CCL11 production and eosinophil infiltration such as
Hodgkin’s lymphoma, nasal polyposis, endometriosis, and allergic
diathesis.
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