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The effects of Th2 cytokines on the expression of ADAM33 in allergen-induced chronic airway inflammation.

Authors: Jie, Z  Jin, M  Cai, Y  Bai, C  Shen, Y  Yuan, Z  Hu, Y  Holgate, S 
Citation: Jie Z, etal., Respir Physiol Neurobiol. 2009 Sep 30;168(3):289-94. Epub 2009 Jul 25.
Pubmed: (View Article at PubMed) PMID:19635592
DOI: Full-text: DOI:10.1016/j.resp.2009.07.019

A disintegrin and metalloprotease domain 33 (ADAM33) has been identified as an asthma susceptibility gene, which is associated with small-airway remodeling. However, the role of ADAM33 in the development of allergic airway inflammation is unclear. The present study used an established murine model of allergen-induced chronic airway inflammation, which was sensitized and then challenged by nebulized 2.5% ovalbumin (OVA) for 8 weeks (30 min/day, three times a week). The expression of ADAM33 mRNA detected by real time RT-PCR was significantly enhanced in the lung tissue of mice with OVA challenge, as compared with the group challenged with saline. This OVA-challenged model showed significant Th2-biased airway inflammation as well as airway remodeling with features of sub-epithelial fibrosis and mucus hyper-secretion. Furthermore, in vitro studies showed that IL-4 and IL-13 could significantly up-regulate the expression of ADAM33 mRNA in human fibroblasts in a concentration- and time-dependent manner as compared to normal controls. These results support the note that Th2 cytokines can up-regulate the expression of ADAM33 mRNA and ADAM33 may play an important role in the development of airway remodeling in allergen-induced chronic airway inflammation.


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CRRD Object Information
CRRD ID: 4145360
Created: 2010-11-01
Species: All species
Last Modified: 2010-11-01
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.