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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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“we suggest that eotaxin-1 release may mediate β-amyloid clearance”
From Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer's disease (2015) · cites this paper as [48]
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Cites
Alessi, D. R., Cuenda, A., Cohen, P., Dudley, D. T., & Saltiel, A. R. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.46.27489 · Cited by 3,374
Identification of a Novel Inhibitor of Mitogen-activated Protein Kinase Kinase
Favata, M. F., Horiuchi, K. Y., Manos, E. J., Daulerio, A. J., Stradley, D. A., Feeser, W. S., Dyk, D. E. V., Pitts, W. J., Earl, R. A., Hobbs, F. W., et al. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.29.18623 · Cited by 3,016
A synthetic inhibitor of the mitogen-activated protein kinase cascade.
Dudley, D. T., Pang, L., Decker, S. J., Bridges, A. J., & Saltiel, A. R. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.17.7686 · Cited by 2,679
Requirement for IL-13 Independently of IL-4 in Experimental Asthma
Grünig, G., Warnock, M. L., Wakil, A. E., Venkayya, R., Brombacher, F., Rennick, D. M., Sheppard, D., Mohrs, M., Donaldson, D. D., Locksley, R. M., et al. (1998) · Science · doi:10.1126/science.282.5397.2261 · Cited by 1,845
Zhu, Z., Homer, R., Wang, Z., Chen, Q., Geba, G. P., Wang, J., Zhang, Y., & Elias, J. A. (1999) · Journal of Clinical Investigation · doi:10.1172/jci5909 · Cited by 1,730
Jose, P. J., Griffiths-Johnson, D. A., COLLINS, P. D., Walsh, D. T., Moqbel, R., Totty, N. F., Truong, O., Hsuan, J. J., & Williams, T. J. (1994) · The Journal of Experimental Medicine · doi:10.1084/jem.179.3.881 · Cited by 806
García-Zepeda, E. A., Rothenberg, M. E., Ownbey, R. T., Celestin, J., Leder, P., & Luster, A. D. (1996) · Nature Medicine · doi:10.1038/nm0496-449 · Cited by 683
Nakajima, T., Kinoshita, S. M., Sasagawa, T., Sasaki, K., Naruto, M., Kishimoto, T., & Akira, S. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.6.2207 · Cited by 573
Inflammation of small airways in asthma☆☆☆★★★
Hamid, Q. A., Song, Y., Kotsimbos, T. C., Minshall, E., Bai, T. R., Hegele, R. G., & Hogg, J. C. (1997) · Journal of Allergy and Clinical Immunology · doi:10.1016/s0091-6749(97)70193-3 · Cited by 548
Targeted Disruption of the Chemokine Eotaxin Partially Reduces Antigen-induced Tissue Eosinophilia
Rothenberg, M. E., MacLean, J. A., Pearlman, E. M., Luster, A. D., & Leder, P. (1997) · The Journal of Experimental Medicine · doi:10.1084/jem.185.4.785 · Cited by 524
Research works printed but not linked: 4
- Bamford TL, 2000, Am J Respir Crit Care Med, 161, A599
- Feng N, 1998, Lab Invest, 78, 591
- Gingras S, 2000, Mol Endocrinol, 14, 229
- Hirst SJ, 2001, Am J Respir Crit Care Med, 163, A513
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May, R. D., Monk, P., Cohen, E. S., Manuel, D. V. F. P., Dempsey, F. C., Davis, N. H. E., Dodd, A., Corkill, D. J., Woods, J. M., Joberty-Candotti, C., et al. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01659.x · Cited by 102
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“ERK phosphorylation is associated with ASM hyperresponsiveness and proliferation (28, 29, 45), leukotriene C4 synthesis (46, 47), IL-13- and IL-4-mediated eotaxin release from ASM cells (48), eotaxin-stimulated eosinophil degranulation (49), and granulocyte-macrophage colony-stimulating factor (GM-CSF) release (50).”
BackgroundInnate Lymphoid Cells Play a Pathogenic Role in Pericarditis
Choi, H. S., Won, T., Hou, X., Chen, G., Bracamonte-Baran, W., Talor, M. V., Jurčová, I., Szárszoi, O., Čurnova, L., Stříž, I., et al. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.02.040 · Cited by 43
Syed, F., Panettieri, R. A., Tliba, O., Huang, C., Li, K. T., Bracht, M., Amegadzie, B. Y., Griswold, D. E., Li, L. Y., & Amrani, Y. (2005) · Respiratory Research · doi:10.1186/1465-9921-6-9 · Cited by 43
“Previous reports using cultured ASM cells also demonstrated that IL-13 can stimulate the expression of other pro-inflammatory proteins, such as eotaxin [8,23,24], TARC [9] or VEGF [25] and tenascin [present report and [10]].”
BackgroundSelf-citationDirect effects of Th2 cytokines on airway smooth muscle
Shore, S. A. (2004) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2004.01.008 · Cited by 43
Self-citationKang, B. N., Jude, J. A., Panettieri, R. A., Walseth, T. F., & Kannan, M. (2008) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00352.2007 · Cited by 43
“, p38, JNK, and ERK, resulting in the regulated expression of a variety of genes involved in excitation-contraction coupling (18, 22, 23, 32, 35, 37, 46, 49, 52).”
BackgroundSelf-citationTranscriptional regulation of cytokine function in airway smooth muscle cells
Clarke, D. L., Damera, G., Sukkar, M. B., & Tliba, O. (2009) · Pulmonary Pharmacology & Therapeutics · doi:10.1016/j.pupt.2009.04.003 · Cited by 41
“Indeed, NF-κB is involved in IL-17-induced IL-8 release [23, 77]; IL-1β and TNF-α-induced GRO-α release [78]; neutrophil-derived elastase-induced TGF-β expression [79]; in the expression of cell adhesion molecules such as ICAM-1 and VCAM-1 induced by TNF-α, IL-1β and LPS [80-82].”
BackgroundInfluentialFujisawa, T., Ide, K., Holtzman, M. J., Suda, T., Suzuki, K., Kuroishi, S., Chida, K., & Nakamura, H. (2008) · Respirology · doi:10.1111/j.1440-1843.2008.01237.x · Cited by 41
Desai, L. P., Wu, Y., Tepper, R. S., & Gunst, S. J. (2011) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00043.2011 · Cited by 39
IL-4 Is Proangiogenic in the Lung under Hypoxic Conditions
Yamaji-Kegan, K., Su, Q., Angelini, D. J., & Johns, R. A. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0713347 · Cited by 39
“IL-4 is also known to initiate activation of MEK subfamilies, including p42/p44 MEK/ERK, in bronchial smooth muscle and epithelial cells (52, 60).”
BackgroundThe role of transcription factors in allergic inflammation
Escoubet‐Lozach, L., Glass, C. K., & Wasserman, S. I. (2002) · Journal of Allergy and Clinical Immunology · doi:10.1067/mai.2002.128076 · Cited by 37
Ablation of Tumor Progression Locus 2 Promotes a Type 2 Th Cell Response in Ovalbumin-Immunized Mice
Watford, W. T., Wang, C.-C., Tsatsanis, C., Mielke, L. A., Eliopoulos, A. G., Daskalakis, C., Charles, N., Odom, S., Rivera, J., O’Shea, J. J., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0803730 · Cited by 38
“eotaxin targets the accumulation of eosinophils at specific sites (25, 28, 29).”
BackgroundInterleukin-4 induces expression of eotaxin in endometriotic stromal cells
Ouyang, Z., Osuga, Y., Hirota, Y., Hirata, T., Yoshino, O., Koga, K., Yano, T., & Taketani, Y. (2009) · Fertility and Sterility · doi:10.1016/j.fertnstert.2009.01.129 · Cited by 38
Interleukin-13 and Interleukin-5 in Induced Sputum of Eosinophilic Bronchitis
Park, S.-W., Jangm, H. K., An, M. H., Min, J. W., Jang, A., Lee, J.-H., & Park, C. (2005) · CHEST Journal · doi:10.1016/s0012-3692(15)52584-1 · Cited by 38
Redhu, N. S., Saleh, A. J., Shan, L., Gerthoffer, W. T., Kung, S. K. P., Halayko, A. J., Lamkhioued, B., & GOUNNI, A. S. (2009) · PLoS ONE · doi:10.1371/journal.pone.0006153 · Cited by 37
“IL-4 plays a critical role in atopic diseases and is also known to cause a marked increase in eotaxin1/CCL11 release in ASM cells [38,39].”
Zhou, J., Wang, C., Wu, J. S., Fukunaga, A., Cheng, Z., Wang, J., Yamauchi, A., Yodoi, J., & Tian, H. (2019) · Antioxidants and Redox Signaling · doi:10.1089/ars.2019.7807 · Cited by 39
“Allergen-specific IgE production by B cells is driven by IL-4, and IL-5 recruits and maintains a large number of EOS in the allergic tissues (18, 89).”
Liang, L., Li, F., Bao, A., Zhang, M., Chung, K. F., & Zhou, X. (2013) · Respirology · doi:10.1111/resp.12189 · Cited by 35
IFN-γ, IL-4 and IL-13 modulate responsiveness of human airway smooth muscle cells to IL-13
Moynihan, B. J., Tolloczko, B., Bassam, S. E., Ferraro, P., Michoud, M.-C., Martin, J. G., & Laberge, S. (2008) · Respiratory Research · doi:10.1186/1465-9921-9-84 · Cited by 35
“The expression of the chemokines eotaxin, eotaxin-3 and TARC is also induced by IL-13, so IL-13 can be linked to the contractile, proliferative and secretory properties of HASM cells [25-27].”
BackgroundEfficacy of an Inhaled IL-13 Antibody Fragment in a Model of Chronic Asthma
Lightwood, D. J., Tservistas, M., Zehentleitner, M., Sarkar, K., Turner, A. V., Bracher, M. G., Smith, B., Lamour, S., Bourne, T., Shaw, S., et al. (2018) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201712-2382oc · Cited by 35
Zuyderduyn, S., Hiemstra, P. S., & Rabe, K. F. (2004) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2004.06.037 · Cited by 35
Knott, M. L., MATTHAEI, K. I., Foster, P., & Dent, L. A. (2009) · Molecular Immunology · doi:10.1016/j.molimm.2009.05.016 · Cited by 34
Modulation of ozone-induced airway hyperresponsiveness and inflammation by interleukin-13
Williams, A. S., Nath, P., Leung, S.-Y., Khorasani, N. M., McKenzie, A. N. J., Adcock, I. M., & Chung, K. F. (2008) · European Respiratory Journal · doi:10.1183/09031936.00121607 · Cited by 34
Ito, I., Laporte, J. D., Fiset, P., Asai, K., Yamauchi, Y., Martin, J. G., & Hamid, Q. A. (2006) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2006.08.038 · Cited by 33
Kirstein, F., Horsnell, W. G. C., Kuperman, D. A., Huang, X., Erle, D. J., Lopata, A. L., & Brombacher, F. (2010) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2010.04.028 · Cited by 33
Sohn, S., Ko, E., Oh, B.-G., Kim, S., Kim, Y., Shin, M., Hong, M., & Bae, H. (2009) · Annals of Allergy Asthma & Immunology · doi:10.1016/s1081-1206(10)60169-x · Cited by 31
Airway Smooth Muscle and Asthma
Oliver, B. G. G., & Black, J. L. (2006) · Allergology International · doi:10.2332/allergolint.55.215 · Cited by 30
Ohnishi, H., Takeda, K., Domenico, J. M., Lucas, J. J., Miyahara, N., Swasey, C. H., Dakhama, A., & Gelfand, E. W. (2009) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2008.10.054 · Cited by 28
Kobayashi, I., Yamamoto, S., Nishi, N., Tsuji, K., Imayoshi, M., Inada, S., Ichiamaru, T., & Hamasaki, Y. (2004) · Annals of Allergy Asthma & Immunology · doi:10.1016/s1081-1206(10)61399-3 · Cited by 28
IFN-γ-induced SOCS-1 regulates STAT6-dependent eotaxin production triggered by IL-4 and TNF-α
Sato, T. A., Saito, R., Jinushi, T., Tsuji, T., Matsuzaki, J., Koda, T., Nishimura, S., Takeshima, H., & Nishimura, T. (2004) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2003.12.124 · Cited by 28
Ennis, D. P., Cassidy, J. P., & Mahon, B. P. (2005) · Clinical and Vaccine Immunology · doi:10.1128/cdli.12.3.409-417.2005 · Cited by 26
“Airway reactivity can be mediated by IgE-independent mechanisms that include a direct influence of IL-4 and IL-13 on airway cells (22, 23, 38, 58).”
BackgroundIL-25 Improves IgA Levels During Parenteral Nutrition Through the JAK-STAT Pathway
Heneghan, A. F., Pierre, J. F., & Kudsk, K. A. (2012) · Annals of Surgery · doi:10.1097/sla.0b013e318277ea9e · Cited by 25
Odaka, M., Matsukura, S., Kuga, H., Kokubu, F., Kasama, T., Kurokawa, M., Kawaguchi, M., Ieki, K., Suzuki, S., Watanabe, S., et al. (2007) · International Archives of Allergy and Immunology · doi:10.1159/000101412 · Cited by 25
“Other chemokine expressions in ASM have been reported, but reports comparing the efficacy of Th1 and Th2 cytokines in induction of chemokines seem few [12–19].”
Monocyte 15-Lipoxygenase Gene Expression Requires ERK1/2 MAPK Activity
Bhattacharjee, A., Mulya, A., Pal, S., Roy, B., Feldman, G. M., & Cathcart, M. K. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1000514 · Cited by 24
Cai, Z., Tian, Y., Li, J.-Z., Zhao, P., Li, J., Mei, X., & Bai, Y. (2022) · Bioscience Reports · doi:10.1042/bsr20220986 · Cited by 23
Punia, N., Smith, S. G., Thomson, J. V., Irshad, A., Nair, P. K., & Sehmi, R. (2011) · Clinical & Experimental Allergy · doi:10.1111/j.1365-2222.2011.03889.x · Cited by 23
Wu, A. Y., Sur, S. A., Grant, J. A., & Tripple, J. W. (2018) · Current Opinion in Allergy and Clinical Immunology · doi:10.1097/aci.0000000000000490 · Cited by 23
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)
- 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 › 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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