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Cited by 166Asthma and respiratory diseasesIL-33, ST2, and ILC PathwaysAllergic Rhinitis and Sensitization

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

Moore, Paul E., Church, Trudi L., Chism, David D., Panettieri, Reynold A., Shore, Stephanie A.·2002·American Journal of Physiology-Lung Cellular and Molecular Physiology
DOI 10.1152/ajplung.00245.2001
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Abstract

Human airway smooth muscle (HASM) cells express interleukin (IL)-13 and IL-4 receptors and respond to these cytokines with signal transducer and activator of transcription-6 and extracellular signal-regulated kinase (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 mitogen-activated protein (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 tumor necrosis factor (TNF)-α to induce eotaxin release: TNF-α alone (10 ng/ml for 24 h) resulted in an approximately fourfold increase in eotaxin release, whereas TNF-α in combination with IL-13 or IL-4 resulted in 10- or 20-fold increases ( P < 0.05). Similar results were obtained for eotaxin mRNA expression. Pretreatment with either U-0126 (10 μM) or PD-98059 (30 μM), both inhibitors of MAP/ERK kinase, the enzyme upstream of ERK, inhibited IL-13- or IL-4-induced eotaxin release ( P < 0.05). U-0126 also inhibited IL-13, and TNF-α 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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Crossref · 10.1152/ajplung.00245.2001

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Research works printed but not linked: 4

  1. Bamford TL, 2000, Am J Respir Crit Care Med, 161, A599
  2. Feng N, 1998, Lab Invest, 78, 591
  3. Gingras S, 2000, Mol Endocrinol, 14, 229
  4. Hirst SJ, 2001, Am J Respir Crit Care Med, 163, A513

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Metadata

Authors
Moore, P. E., Church, T. L., Chism, D. D., Panettieri, R. A., & Shore, S. A.
Affiliations
  • Harvard University (US)
  • University of Pennsylvania (US)
ORCID
Venue
American Journal of Physiology-Lung Cellular and Molecular Physiology
Publisher
American Physiological Society
Published
2002-04-01
Volume
282
Issue
4
Pages
L847-L853
ISSN
  • 1040-0605 (ISSN-L)
  • 1522-1504
DOI
10.1152/ajplung.00245.2001
OpenAlex
W2150773437
Cited by
166
References
49
Citations by year
2026: 1 · 2025: 6 · 2024: 4 · 2023: 7 · 2022: 5 · 2021: 3 · 2020: 2 · 2019: 6 · 2018: 6 · 2017: 2 · 2016: 5 · 2015: 4 · 2014: 3 · 2013: 9 · 2012: 5
FWCI
8.61
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p50hl056383-06)
  • National Heart, Lung, and Blood Institute (HL04395, P01HL033009, HL-33009, HL 56383, K08HL004395)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
  • Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
Keywords
IL-13, IL-4, eotaxin, CCL17, airway smooth muscle cells, ERK activation, MAPK signaling, TNF-α, chemokine secretion, eosinophil recruitment, asthma, U0126, PD98059
MeSH terms
Antineoplastic Agents, Asthma, Butadienes, Cells, Cultured, Enzyme Inhibitors, Flavonoids, Humans, Muscle, Smooth, Nitriles, RNA, Messenger, Trachea, Tumor Necrosis Factor-alpha, Interleukin-4, Gene Expression, Interleukin-13, Chemokines, CC, Mitogen-Activated Protein Kinases, Chemokine CCL11

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