TY - JOUR
TI - Implication of Interleukin (IL)-18 in the pathogenesis of chronic obstructive pulmonary disease (COPD)
AU - Dima, E.
AU - Koltsida, O.
AU - Katsaounou, P.
AU - Vakali, S.
AU - Koutsoukou, A.
AU - Koulouris, N.G.
AU - Rovina, N.
JO - Cytokine
PY - 2015
VL - 74
TODO - 2
SP - 313-317
PB - INSTAP Academic Press
SN - 1043-4666, 1096-0023
TODO - 10.1016/j.cyto.2015.04.008
TODO - 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
TODO - 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.
ER -