Τίτλος:
Implication of Interleukin (IL)-18 in the pathogenesis of chronic obstructive pulmonary disease (COPD)
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
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.
Συγγραφείς:
Dima, E.
Koltsida, O.
Katsaounou, P.
Vakali, S.
Koutsoukou, A.
Koulouris, N.G.
Rovina, N.
Εκδότης:
INSTAP Academic Press
Λέξεις-κλειδιά:
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
DOI:
10.1016/j.cyto.2015.04.008
