Cysteinyl leukotriene upregulates IL-11 expression in allergic airway disease of mice

Kyung Sun Lee, So Ri Kim, Hee Sun Park, Seoung Ju Park, Kyung-Hoon Min, Ka Young Lee, Sun Mi Jin, Yong Chul Lee

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Background: Chronic airway inflammation and airway remodeling are important features of bronchial asthma. IL-11 is one of the important mediators involved in the process of airway inflammation and remodeling. Cysteinyl leukotrienes (cysLTs) play roles in recruitment of inflammatory cells, airway smooth muscle contraction, vascular leakage, increased mucus secretion, decreased mucociliary clearance, and airway fibrosis. Objective: An aim of the present study was to determine the effect of the cysLTs on the regulation of IL-11 expression. Methods: We used a C57BL/6 mouse model of allergic airway disease and murine tracheal epithelial cells to examine the effects of cysLTs on the regulation of IL-11 expression. Results: Our present study with an ovalbumin-induced murine model of allergic airway disease revealed that levels of leukotriene C4 (LTC4) in bronchoalveolar lavage fluids were increased and that administration of montelukast or pranlukast reduced the increased levels of LTC4; the increased expression of IL-11 protein and mRNA in lung tissues; airway inflammation, bronchial hyperresponsiveness; the increased levels of TGF-β1, IL-4, and IL-13 in bronchoalveolar lavage fluids and lung tissues; and airway fibrosis. In addition, LTC4 stimulates epithelial cells to produce IL-11. Our results also showed that cysLT type 1 receptor antagonists downregulated the activity of a transcription factor, nuclear factor κB, and BAY 11-7085 substantially reduced the increased levels of IL-11 after ovalbumin inhalation. Conclusion: These results suggest that cysLTs regulate the IL-11 expression in allergic airway disease. Clinical implications: These findings provide one of the molecular mechanisms for the effects of cysLTs on airway inflammation and fibrosis in allergic airway diseases.

Original languageEnglish
Pages (from-to)141-149
Number of pages9
JournalJournal of Allergy and Clinical Immunology
Volume119
Issue number1
DOIs
Publication statusPublished - 2007 Jan 1
Externally publishedYes

Fingerprint

Interleukin-11
Up-Regulation
Leukotriene C4
Inflammation
Airway Remodeling
Fibrosis
montelukast
Ovalbumin
Bronchoalveolar Lavage Fluid
Tracheal Diseases
Epithelial Cells
Mucociliary Clearance
Lung
Interleukin-13
Mucus
Muscle Contraction
cysteinyl-leukotriene
Inbred C57BL Mouse
Interleukin-4
Inhalation

Keywords

  • airway
  • Cysteinyl leukotrienes
  • IL-11
  • inflammation
  • remodeling

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Cysteinyl leukotriene upregulates IL-11 expression in allergic airway disease of mice. / Lee, Kyung Sun; Kim, So Ri; Park, Hee Sun; Park, Seoung Ju; Min, Kyung-Hoon; Lee, Ka Young; Jin, Sun Mi; Lee, Yong Chul.

In: Journal of Allergy and Clinical Immunology, Vol. 119, No. 1, 01.01.2007, p. 141-149.

Research output: Contribution to journalArticle

Lee, Kyung Sun ; Kim, So Ri ; Park, Hee Sun ; Park, Seoung Ju ; Min, Kyung-Hoon ; Lee, Ka Young ; Jin, Sun Mi ; Lee, Yong Chul. / Cysteinyl leukotriene upregulates IL-11 expression in allergic airway disease of mice. In: Journal of Allergy and Clinical Immunology. 2007 ; Vol. 119, No. 1. pp. 141-149.
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AU - Park, Hee Sun

AU - Park, Seoung Ju

AU - Min, Kyung-Hoon

AU - Lee, Ka Young

AU - Jin, Sun Mi

AU - Lee, Yong Chul

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AB - Background: Chronic airway inflammation and airway remodeling are important features of bronchial asthma. IL-11 is one of the important mediators involved in the process of airway inflammation and remodeling. Cysteinyl leukotrienes (cysLTs) play roles in recruitment of inflammatory cells, airway smooth muscle contraction, vascular leakage, increased mucus secretion, decreased mucociliary clearance, and airway fibrosis. Objective: An aim of the present study was to determine the effect of the cysLTs on the regulation of IL-11 expression. Methods: We used a C57BL/6 mouse model of allergic airway disease and murine tracheal epithelial cells to examine the effects of cysLTs on the regulation of IL-11 expression. Results: Our present study with an ovalbumin-induced murine model of allergic airway disease revealed that levels of leukotriene C4 (LTC4) in bronchoalveolar lavage fluids were increased and that administration of montelukast or pranlukast reduced the increased levels of LTC4; the increased expression of IL-11 protein and mRNA in lung tissues; airway inflammation, bronchial hyperresponsiveness; the increased levels of TGF-β1, IL-4, and IL-13 in bronchoalveolar lavage fluids and lung tissues; and airway fibrosis. In addition, LTC4 stimulates epithelial cells to produce IL-11. Our results also showed that cysLT type 1 receptor antagonists downregulated the activity of a transcription factor, nuclear factor κB, and BAY 11-7085 substantially reduced the increased levels of IL-11 after ovalbumin inhalation. Conclusion: These results suggest that cysLTs regulate the IL-11 expression in allergic airway disease. Clinical implications: These findings provide one of the molecular mechanisms for the effects of cysLTs on airway inflammation and fibrosis in allergic airway diseases.

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KW - remodeling

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