Modulation of bronchial epithelial cells by IL-17

Mio Kawaguchi, Fumio Kokubu, Hideki Kuga, Satoshi Matsukura, Hiroshi Hoshino, Koushi Ieki, Toshimichi Imai, Mitsuru Adachi, Shau Ku Huang

Research output: Contribution to journalArticle

124 Citations (Scopus)

Abstract

Background: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. Objective: To determine the role of IL-17, a CD4+T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. Methods: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. Results: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-γ further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-γ augmented IL-6 and ICAM-1 expression. Conclusion: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via - in part - the expression of epithelial IL-6, IL-8, and ICAM-1.

Original languageEnglish
Pages (from-to)804-809
Number of pages6
JournalJournal of Allergy and Clinical Immunology
Volume108
Issue number5
DOIs
Publication statusPublished - Jan 1 2001
Externally publishedYes

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Interleukin-17
Epithelial Cells
Interleukin-8
Intercellular Adhesion Molecule-1
Interleukin-6
Mitogen-Activated Protein Kinases
Cytokines
Interleukin-13
Chemokines
Interleukin-4
MAP Kinase Kinase 4
Chemokine CCL5
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase Kinases
Protein Kinase Inhibitors
Leukocytes
Western Blotting
Enzyme-Linked Immunosorbent Assay
Inflammation

Keywords

  • Adhesion molecule
  • Bronchial epithelial cell
  • ERKl/2
  • Interleukin-17
  • Interleukin-6
  • Interleukin-8

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Kawaguchi, M., Kokubu, F., Kuga, H., Matsukura, S., Hoshino, H., Ieki, K., ... Huang, S. K. (2001). Modulation of bronchial epithelial cells by IL-17. Journal of Allergy and Clinical Immunology, 108(5), 804-809. https://doi.org/10.1067/mai.2001.119027

Modulation of bronchial epithelial cells by IL-17. / Kawaguchi, Mio; Kokubu, Fumio; Kuga, Hideki; Matsukura, Satoshi; Hoshino, Hiroshi; Ieki, Koushi; Imai, Toshimichi; Adachi, Mitsuru; Huang, Shau Ku.

In: Journal of Allergy and Clinical Immunology, Vol. 108, No. 5, 01.01.2001, p. 804-809.

Research output: Contribution to journalArticle

Kawaguchi, M, Kokubu, F, Kuga, H, Matsukura, S, Hoshino, H, Ieki, K, Imai, T, Adachi, M & Huang, SK 2001, 'Modulation of bronchial epithelial cells by IL-17', Journal of Allergy and Clinical Immunology, vol. 108, no. 5, pp. 804-809. https://doi.org/10.1067/mai.2001.119027
Kawaguchi M, Kokubu F, Kuga H, Matsukura S, Hoshino H, Ieki K et al. Modulation of bronchial epithelial cells by IL-17. Journal of Allergy and Clinical Immunology. 2001 Jan 1;108(5):804-809. https://doi.org/10.1067/mai.2001.119027
Kawaguchi, Mio ; Kokubu, Fumio ; Kuga, Hideki ; Matsukura, Satoshi ; Hoshino, Hiroshi ; Ieki, Koushi ; Imai, Toshimichi ; Adachi, Mitsuru ; Huang, Shau Ku. / Modulation of bronchial epithelial cells by IL-17. In: Journal of Allergy and Clinical Immunology. 2001 ; Vol. 108, No. 5. pp. 804-809.
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abstract = "Background: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. Objective: To determine the role of IL-17, a CD4+T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. Methods: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. Results: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-γ further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-γ augmented IL-6 and ICAM-1 expression. Conclusion: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via - in part - the expression of epithelial IL-6, IL-8, and ICAM-1.",
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AU - Kokubu, Fumio

AU - Kuga, Hideki

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AU - Hoshino, Hiroshi

AU - Ieki, Koushi

AU - Imai, Toshimichi

AU - Adachi, Mitsuru

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N2 - Background: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. Objective: To determine the role of IL-17, a CD4+T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. Methods: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. Results: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-γ further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-γ augmented IL-6 and ICAM-1 expression. Conclusion: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via - in part - the expression of epithelial IL-6, IL-8, and ICAM-1.

AB - Background: The induction of epithelial cytokines/chemokines is crucial in the migration of leukocytes, and its regulatory mechanisms remain incompletely defined. Objective: To determine the role of IL-17, a CD4+T cell-derived cytokine, in modulation of primary bronchial epithelial cells, the expression of IL-6, IL-8, and intercellular adhesion molecule 1 (ICAM-1) and the potential involvement of mitogen-activated protein (MAP) kinases in IL-17-mediated signaling were examined. Methods: The levels of gene expression and protein production for IL-6 and IL-8 in IL-17-treated cells, in the presence or absence of MAP kinase inhibitors, were analyzed by RT-PCR and ELISA, respectively, and activation of MAP kinases was determined by Western blot analyses. Results: We showed first that IL-17 induced time-dependent expression of IL-6 and IL-8 but not of the chemokines eotaxin and RANTES. In addition, IL-17 induced activation of extracellular signal-regulated kinase 1/2 but not of p38 or JNK kinases. A selective MAP kinase kinase inhibitor, PD98059, inhibited IL-17-induced IL-6 and IL-8. A combination of IL-17 and each of the cytokines IL-4, IL-13, and IFN-γ further enhanced IL-8 expression. IL-17 alone did not induce ICAM-1 expression and showed no effect on IL-4- or IL-13-induced ICAM-1 expression. In contrast, a combination of IL-17 and IFN-γ augmented IL-6 and ICAM-1 expression. Conclusion: These findings suggest that IL-17, alone or in combination with other cytokines, modulates airway inflammation via - in part - the expression of epithelial IL-6, IL-8, and ICAM-1.

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KW - Interleukin-6

KW - Interleukin-8

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