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Am J Physiol Lung Cell Mol Physiol (November 30, 2001). doi:10.1152/ajplung.00321.2001
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Articles in PresS, published online ahead of print November 30, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00321.2001
Submitted on August 13, 2001
Accepted on November 27, 2001

Th2 Cytokine Regulation of Type I Collagen Gel Contraction Mediated by Human Lung Mesenchymal Cells

Xiangde Liu1, Tadashi Kohyama1, Hangjun Wang2, Yun K Zhu3, Fu-Qiang Wen1, Huizhong Kim1, Debra J Romberger1, and Stephen I Rennard1*

1 Pulmonary and Critical Care Medicine, University of Nebraska Medical Center, Omaha, NE, USA
2 Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada
3 Respiratory Diseases, Jincheng Hospital, Lanzhou, China

* To whom correspondence should be addressed. E-mail: srennard{at}unmc.edu.

Asthma is characterized by chronic inflammation of the airway wall with the presence of activated Th2 lymphocytes. The current study assessed the ability of Th2 cytokines to modulate fibroblast-mediated contraction of collagen gels in order to determine if Th2 cytokines could contribute to tissue remodeling by altering mesenchymal cell contraction. Human fetal lung fibroblasts, human adult bronchial fibroblasts and human airway smooth muscle cells were cast into native type I collagen gels and allowed to contract in the presence or absence of IL-4, IL-5, IL-10 or IL-13. IL-4 and IL-13 but not IL-5 and IL-10 augmented collagen gel contraction in a concentration-dependent manner. Neither IL-4 nor IL-13 altered fibroblast production of TGF-ßor fibronectin. Both, however, decreased fibroblast PGE2 release. Decreased PGE2 release was associated with a decreased expression of cyclooxygenase 1 and 2 protein and mRNA. Indomethacin completely inhibited PGE release and also augmented contraction. IL-4 and IL-13, however, added together with indomethacin further augmented contraction suggesting both a PGE-dependent and a PGE-independent effect. These findings suggest that IL-4 and IL-13 may modulate airway tissue remodeling and, therefore, could play a role in the altered airway connective tissue which characterizes asthma.




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