BioSpace Collaborative

Academic/Biomedical Research
News & Jobs
Biotechnology and Pharmaceutical Channel Medical Device and Diagnostics Channel Clinical Research Channel BioSpace Collaborative    Job Seekers:  Register | Login          Employers:  Register | Login  

Free Newsletters
My Subscriptions

News by Subject
News by Disease
News by Date
Search News
Post Your News

Job Seeker Login
Most Recent Jobs
Search Jobs
Post Resume
Career Fairs
Career Resources
For Employers

Regional News
US & Canada
  Biotech Bay
  Biotech Beach
  Pharm Country
  Bio NC
  Southern Pharm
  BioCanada East
  C2C Services & Suppliers™


Company Profiles

Research Store

Research Events
Post an Event
Real Estate
Business Opportunities

PLoS By Category | Recent PLoS Articles
Otolaryngology - Respiratory Medicine

Clara Cell 10-kDa Protein Gene Transfection Inhibits NF-?B Activity in Airway Epithelial Cells
Published: Wednesday, April 25, 2012
Author: Xiao-Bo Long et al.

by Xiao-Bo Long, Shuang Hu, Nan Wang, Hong-Tao Zhen, Yong-Hua Cui, Zheng Liu


Clara cell 10-kDa protein (CC10) is a multifunctional protein with anti-inflammatory and immunomodulatory effects. Induction of CC10 expression by gene transfection may possess potential therapeutic effect. Nuclear factor ?B (NF-?B) plays a key role in the inflammatory processes of airway diseases.


To investigate potential therapeutic effect of CC10 gene transfection in controlling airway inflammation and the underlying intracellular mechanisms, in this study, we constructed CC10 plasmid and transfected it into bronchial epithelial cell line BEAS-2B cells and CC10 knockout mice. In BEAS-2B cells, CC10's effect on interleukin (IL)-1ß induced IL-8 expression was explored by means of RT-PCR and ELISA and its effect on NF-?B classical signaling pathway was studied by luciferase reporter, western blot, and immunoprecipitation assay. The effect of endogenous CC10 on IL-1ß evoked IL-8 expression was studied by means of nasal explant culture. In mice, CC10's effect on IL-1ß induced IL-8 and nuclear p65 expression was examined by immunohistochemistry. First, we found that the CC10 gene transfer could inhibit IL-1ß induced IL-8 expression in BEAS-2B cells. Furthermore, we found that CC10 repressed IL-1ß induced NF-?B activation by inhibiting the phosphorylation of I?B-a but not I?B kinase-a/ß in BEAS-2B cells. Nevertheless, we did not observe a direct interaction between CC10 and p65 subunit in BEAS-2B cells. In nasal explant culture, we found that IL-1ß induced IL-8 expression was inversely correlated with CC10 levels in human sinonasal mucosa. In vivo study revealed that CC10 gene transfer could attenuate the increase of IL-8 and nuclear p65 staining in nasal epithelial cells in CC10 knockout mice evoked by IL-1ß administration.


These results indicate that CC10 gene transfer may inhibit airway inflammation through suppressing the activation of NF-?B, which may provide us a new consideration in the therapy of airway inflammation.