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Blood, 15 January 2002, Vol. 99, No. 2, pp. 538-545
IMMUNOBIOLOGY
Increased and prolonged inflammation and angiogenesis in
delayed-type hypersensitivity reactions elicited in the skin of
thrombospondin-2-deficient mice
Bernhard Lange-Asschenfeldt,
Wolfgang Weninger,
Paula Velasco,
Themis R. Kyriakides,
Ulrich H. von
Andrian,
Paul Bornstein, and
Michael Detmar
From the Cutaneous Biology Research Center, Department
of Dermatology, Massachusetts General Hospital and Harvard Medical
School, Charlestown, MA; the Center for Blood Research and the
Department of Pathology, Harvard Medical School, Boston, MA; and the
Department of Biochemistry, University of Washington, Seattle.
Angiogenesis and enhanced microvascular permeability are hallmarks
of a large number of inflammatory diseases. Although up-regulation of
proangiogenic factors such as vascular endothelial growth factor and
interleukin-8 have been previously reported in inflamed tissue, the
biologic role of endogenous inhibitors of angiogenesis in inflammation
has remained unclear. To investigate the biologic role of the potent
angiogenesis inhibitor thrombospondin-2 (TSP-2) in the control of
cutaneous inflammation, delayed-type hypersensitivity reactions were
elicited in the ear skin of wild-type and TSP-2-deficient mice by
topical sensitization and challenge with oxazolone. Cutaneous TSP-2
expression was up-regulated in the inflamed skin of wild-type mice,
predominantly in dermal fibroblasts and microvessels. Lack of TSP-2
resulted in a significantly enhanced inflammatory response with
increased angiogenesis, edema formation, and inflammatory infiltration.
Ear swelling and inflammation persisted for more than 2 weeks in
TSP-2-deficient mice, as compared with 1 week in wild-type mice.
Although baseline vascular permeability was unchanged, significantly
enhanced microvascular leakage was found in the inflamed skin of
TSP-2-deficient mice. Moreover, the fraction of rolling leukocytes was
significantly increased in the untreated skin of TSP-2-deficient mice.
These results reveal an important role of TSP-2 in limiting the extent
and the duration of edema formation, angiogenesis, and inflammatory
cell infiltration during acute and chronic inflammation.
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