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Cutting Edge |
*
Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224;
Division of Allergy, Asthma, and Rheumatology, Department of Pediatrics, Chang Gung Children’s Hospital, Taoyuan, Taiwan, Republic of China; and
National Institute of Child Health and Development, National Institutes of Health, Bethesda, MD 20892
Clara cell secretory protein (CC10) is a steroid-inducible
protein, and its in vivo function is currently unclear. The role of
CC10 in modulation of pulmonary allergic inflammation was examined in
mice deficient for the CC10 gene. Wild-type and
homozygous CC10-deficient mice were sensitized with an Ag, OVA, and
challenged with either OVA or saline. When compared with that seen in
wild-type mice, a significantly higher level of pulmonary
eosinophilia was found in Ag-sensitized and challenged
CC10-deficient mice. Significantly increased levels of Th2 cytokines
IL-4, IL-5, IL-9, and IL-13 were also found in CC10-deficient mice. In
addition, an increased level of eotaxin, but not RANTES, was also seen
in CC10-deficient mice. No significant difference was observed in the
level of a Th1 cytokine, IFN-
, between different groups of mice.
These results provided the first in vivo evidence that CC10 plays a
role in the modulation of pulmonary allergic
inflammation.
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