Involvement of cystic fibrosis transmembrane conductance regulator in infection-induced edema

Authors

  • Louis Chukwuemeka Ajonuma,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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    • Present address: Oral Bioscience, Faculty of Dentistry, The University of Hong Kong, Hong Kong.

  • Qiong He,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Paul Kay Sheung Chan,

    1. Department of Microbiology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Ernest Hung Yu Ng,

    1. Department of Obstetrics & Gynecology, University of Hong Kong, Pokfulam, Hong Kong
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  • Kin Lam Fok,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Connie Hau Yan Wong,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Lai Ling Tsang,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Lok Sze Ho,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Miu Ching Lau,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Hong Yi Huang,

    1. Department of Obstetrics & Gynecology, Second Affiliated Hospital of Sun Yat-Sen University, Guang Zhuo, P.R. China
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  • Dong Zi Yang,

    1. Department of Obstetrics & Gynecology, Second Affiliated Hospital of Sun Yat-Sen University, Guang Zhuo, P.R. China
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  • Dewi Kenneth Rowlands,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Xiao Xiao Tang,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Xiao Hu Zhang,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Yiu Wa Chung,

    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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  • Hsiao Chang Chan

    Corresponding author
    1. Epithelial Cell Biology Research Center, Li Ka Shing Institute of Health Science, Department of Physiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong
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Corresponding author. Tel: +852 2609 6839; fax: +852 2603 5022. hsiaocchan@cuhk.edu.hk

Abstract

Abnormal fluid accumulation in tissues, including the life-threatening cerebral and pulmonary edema, is a severe consequence of bacteria infection. Chlamydia (C.) trachomatis is an obligate intracellular gram-negative human pathogen responsible for a spectrum of diseases, causing tissue fluid accumulation and edema in various organs. However, the underlying mechanism for tissue fluid secretion induced by C. trachomatis and most of other infectious pathogens is not known. Here, we report that in mice C. trachomatis infection models, the expression of cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP activated chloride channel, is up regulated together with increased cytokine release and tissue fluid accumulation that can be reversed by treatment with antibiotic specific for C. trachomatis and CFTR channel blocker. However, C. trachomatis infection cannot induce tissue edema in CFTR tm1Unc mutant mice. Administration of exogenous IL-1β to mice mimics the C. trachomatis infection-induced CFTR upregulation, enhanced CFTR channel activity and fluid accumulation, further confirming the involvement of CFTR in infection-induced tissue fluid secretion.

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