Cutting edge: Altered pulmonary eosinophilic inflammation in mice deficient for clara cell secretory 10-kDa protein

L. C. Chen, Z. Zhang, A. C. Myers, S. K. Huang

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

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-γ 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.

Original languageEnglish
Pages (from-to)3025-3028
Number of pages4
JournalJournal of Immunology
Volume167
Issue number6
DOIs
Publication statusPublished - Sep 15 2001
Externally publishedYes

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Pneumonia
Proteins
Uteroglobin
Interleukin-9
Pulmonary Eosinophilia
Cytokines
Chemokine CCL5
Interleukin-13
Interleukin-5
Interleukin-4
Steroids
Genes

ASJC Scopus subject areas

  • Immunology

Cite this

Cutting edge : Altered pulmonary eosinophilic inflammation in mice deficient for clara cell secretory 10-kDa protein. / Chen, L. C.; Zhang, Z.; Myers, A. C.; Huang, S. K.

In: Journal of Immunology, Vol. 167, No. 6, 15.09.2001, p. 3025-3028.

Research output: Contribution to journalArticle

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