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Involvement of cystic fibrosis transmembrane conductance regulator in infection‐induced edema
Author(s) -
Ajonuma Louis Chukwuemeka,
He Qiong,
Chan Paul Kay Sheung,
Ng Ernest Hung Yu,
Fok Kin Lam,
Wong Connie Hau Yan,
Tsang Lai Ling,
Ho Lok Sze,
Lau Miu Ching,
Huang Hong Yi,
Yang Dong Zi,
Rowlands Dewi Kenneth,
Tang Xiao Xiao,
Zhang Xiao Hu,
Chung Yiu Wa,
Chan Hsiao Chang
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.03.010
Subject(s) - cystic fibrosis transmembrane conductance regulator , chlamydia trachomatis , secretion , chloride channel , cystic fibrosis , edema , microbiology and biotechnology , biology , intracellular , immunology , chemistry , medicine , endocrinology , genetics
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.