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Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop.

Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Research Abstract Details 

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  • Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Abstract Text:

    yin chenYin Chen,philip thaiPhilip Thai,yu-hua zhaoYu-Hua Zhao,ye-shih hoYe-Shih Ho,mary m desouzaMary M DeSouza,reen wuReen Wu,

    Mucus hypersecretion and persistent airway inflammation are common features of various airway diseases, such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis. One key question is: does the associated airway inflammation in these diseases affect mucus production? If so, what is the underlying mechanism? It appears that increased mucus secretion results from increased mucin gene expression and is also frequently accompanied by an increased number of mucous cells (goblet cell hyperplasia/metaplasia) in the airway epithelium. Many studies on mucin gene expression have been directed toward Th2 cytokines such as interleukin (IL)-4, IL-9, and IL-13 because of their known pathophysiological role in allergic airway diseases such as asthma. However, the effect of these cytokines has not been definitely linked to their direct interaction with airway epithelial cells. In our study, we treated highly differentiated cultures of primary human tracheobronchial epithelial (TBE) cells with a panel of cytokines (interleukin-1alpha, 1beta, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 15, 16, 17, 18, and tumor necrosis factor alpha). We found that IL-6 and IL-17 could stimulate the mucin genes, MUC5B and MUC5AC. The Th2 cytokines IL-4, IL-9, and IL-13 did not stimulate MUC5AC or MUC5B in our experiments. A similar stimulation of MUC5B/Muc5b expression by IL-6 and IL-17 was demonstrated in primary monkey and mouse TBE cells. Further investigation of MUC5B expression demonstrated that IL-17's effect is at least partly mediated through IL-6 by a JAK2-dependent autocrine/paracrine loop. Finally, evidence is presented to show that both IL-6 and IL-17 mediate MUC5B expression through the ERK signaling pathway.

    Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Publishing Authors By Initials

    y chenY Chen,p thaiP Thai,yh zhaoYH Zhao,ys hoYS Ho,mm desouzaMM DeSouza,r wuR Wu,

    For similar respiratory system: respiratory mucosa research abstracts see: respiratory system: respiratory mucosa research

    PUBMED ID PMID:

    MEDLINE DATE:

    Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: The Journal of biological chemistry

    VOLUME: 278

    Page Numbers: 17036-43

    Journal Abbreviation: J. Biol. Chem.

    ISSN: 0021-9258

    DAY: 6

    MONTH: 03

    YEAR: 2003

    Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985121

    Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Keywords Mesh Terms:

    KEYWORDS: Respiratory Mucosa

    MESH TERMS: physiology

    Chemical & Substance for Abstract: Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop. Information

    Substance Name: mucin 5AC

    Registry Number: 0

    Grant and Affiliation Information for Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop.

    AFFILIATION: Center for Comparative Respiratory Biology and Medicine, University of California, Davis, California 95616, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL35635

    ACRONYM: HL

    MEDLINETA: J Biol Chem

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    ACCESSION NUMBER:

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