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Blood, Vol. 95 No. 1 (January 1), 2000:
pp. 263-269
Inhibition of eosinophilic inflammation in allergen-challenged,
IL-1 receptor type 1-deficient mice is associated with reduced
eosinophil rolling and adhesion on vascular endothelium
David H. Broide,
Keith Campbell,
Tim Gifford, and
P. Sriramarao
From the Department of Medicine, University of California, San
Diego; and the Laboratory of Immunology and Vascular
Biology, La Jolla Institute for Experimental Medicine, La
Jolla, CA.
To determine the relative in vivo importance of IL-1 release after
allergen challenge to the subsequent endothelial adhesion and
recruitment of eosinophils, the authors used ovalbumin sensitization and inhalation challenge to induce airway eosinophilia in IL-1 receptor
type 1-deficient and control wild-type mice. Bronchoalveolar lavage
(BAL) eosinophil recruitment in IL-1 receptor type 1-deficient mice
challenged with ovalbumin (24.3% ± 6.3% BAL eosinophils) was
significantly reduced compared with wild-type mice (63.7% ± 2.5%
BAL eosinophils). To determine whether the inhibition of eosinophil
adhesion to vascular endothelium contributed to the inhibition of
eosinophil recruitment in IL-1 receptor type 1-deficient mice, the
authors used intravital microscopy to visualize the rolling and firm
adhesion of fluorescence-labeled mouse eosinophils in the
microvasculature of the allergen-challenged mouse mesentery. Eosinophil
rolling, eosinophil firm adhesion to endothelium, and transmigration
across endothelium (peritoneal eosinophils) were significantly
inhibited in allergen-challenged IL-1 receptor type 1-deficient mice
compared with wild-type mice. Overall, these studies demonstrate that
cytokines such as IL-1, released after allergen challenge, are
important in the induction of endothelial cell adhesiveness, a
prerequisite for the recruitment of circulating eosinophils. (Blood.
2000;95:263-269)

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