IL-13 and IL-4 cause eotaxin release in human airway smooth muscle cells: a role for ERK
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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- Authors
- Moore, P. E., Church, T. L., Chism, D. D., Panettieri, R. A., & Shore, S. A.
- Affiliations
- Harvard University (US)
- University of Pennsylvania (US)
- 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
- 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 › Physiology › 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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