@article{3003784,
    title = "Implication of Interleukin (IL)-18 in the pathogenesis of chronic obstructive pulmonary disease (COPD)",
    author = "Dima, E. and Koltsida, O. and Katsaounou, P. and Vakali, S. and Koutsoukou, A. and Koulouris, N.G. and Rovina, N.",
    journal = "Cytokine",
    year = "2015",
    volume = "74",
    number = "2",
    pages = "313-317",
    publisher = "INSTAP Academic Press",
    issn = "1043-4666, 1096-0023",
    doi = "10.1016/j.cyto.2015.04.008",
    keywords = "colony stimulating factor 1;  cryopyrin;  gamma interferon;  inflammasome;  interleukin 17;  interleukin 18;  purinergic P2X7 receptor;  interleukin 18;  interleukin 18 protein, human;  interleukin 1beta converting enzyme, CD8+ T lymphocyte;  chronic obstructive lung disease;  cytokine release;  cytokine response;  disease association;  disease severity;  forced expiratory volume;  forced vital capacity;  human;  immune response;  infection sensitivity;  inflammation;  nonhuman;  pathophysiology;  priority journal;  protein expression;  protein localization;  respiratory tract infection;  Review;  smoking;  upregulation;  animal;  dendritic cell;  disease model;  helper cell;  immunology;  lung;  macrophage;  mouse;  pathology;  Pulmonary Disease, Chronic Obstructive, Animals;  Caspase 1;  Dendritic Cells;  Disease Models, Animal;  Humans;  Interleukin-18;  Lung;  Macrophages;  Mice;  Pulmonary Disease, Chronic Obstructive;  T-Lymphocytes, Helper-Inducer",
    abstract = "Interleukin (IL)-18 is a pro-inflammatory cytokine that was firstly described as an interferon (IFN)-γ-inducing factor. Similar to IL-1β, IL-18 is synthesized as an inactive precursor requiring processing by caspase-1 into an active cytokine. The platform for activating caspase-1 is known as the inflammasome, a multiple protein complex. Macrophages and dendritic cells are the primary sources for the release of active IL-18, whereas the inactive precursor remains in the intracellular compartment of mesenchymal cells. Finally, the IL-18 precursor is released from dying cells and processed extracellularly.IL-18 has crucial host defense and antitumor activities, and gene therapy to increase IL-18 levels in tissues protects experimental animals from infection and tumor growth and metastasis. Moreover, multiple studies in experimental animal models have shown that IL-18 over-expression results to emphysematous lesions in mice. The published data prompt to the hypothesis that IL-18 induces a broad spectrum of COPD-like inflammatory and remodeling responses in the murine lung and also induces a mixed type 1, type 2, and type 17 cytokine responses. The majority of studies identify IL-18 as a potential target for future COPD therapeutics to limit both the destructive and remodeling processes occurring in COPD lungs. © 2015 Elsevier Ltd."
}