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Am J Physiol Lung Cell Mol Physiol (November 16, 2001). doi:10.1152/ajplung.00245.2001
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Articles in PresS, published online ahead of print November 16, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00245.2001
Submitted on July 2, 2001
Accepted on November 13, 2001

IL-13 and IL-4 cause eotaxin release in human airway smooth muscle cells: a role for ERK

Paul E Moore1, Trudi L Church1, David D Chism1, Reynold A Panettieiri2, and Stephanie A Shore1*

1 Physiology Program, Harvard School of Public Health, Boston, MA, USA
2 Pulmonary and Critical Care Medicine, University of Pennsylvania, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.

Human airway smooth muscle (HASM) cells express IL-13 and IL-4 receptors and respond to these cytokines with STAT-6 and ERK activation. The purpose of this study was to determine whether IL-13 and/or IL-4 influence eotaxin release in HASM cells and whether the ERK MAP kinase pathway is involved in these events. Eotaxin release into HASM cell supernatants was assayed by ELISA, and eotaxin mRNA expression was determined by Northern blot analysis. Pretreatment with either IL-13 or IL-4 resulted in a concentration- and time-dependent release of eotaxin, although IL-4 was more effective. Eotaxin release was approximately twice baseline after treatment with 50 ng/ml IL-13 or IL-4 (p<0.001). IL-13 and IL-4 also acted synergistically with TNF{alpha} to induce eotaxin release: TNF{alpha} alone (10 ng/ml for 24 h) resulted in an ~4-fold increase in eotaxin release, whereas TNF{alpha} in combination with IL-13 or IL-4 resulted in 10-fold or 20-fold increases (p<0.05). Similar results were obtained for eotaxin mRNA expression. Pretreatment with either U0126 (10 µM) or PD98059 (30 µM), both inhibitors of MEK, the enzyme upstream of ERK, inhibited IL-13 or IL-4 induced eotaxin release (p<0.05). U0126 also inhibited IL-13 and TNF{alpha} induced mRNA expression. Our results indicate that IL-13 and IL-4 cause eotaxin release in HASM cells through a mechanism that, in part, involves ERK activation and suggest that the smooth muscle may be an important source of chemokines leading to eosinophil recruitment in asthma.




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