The role of apoptosis in the pathophysiology of Acute Respiratory Distress Syndrome (ARDS): An up-to-date cell-specific review (Journal article)

Galani, V./ Tatsaki, E./ Bai, M./ Kitsoulis, P./ Lekka, M./ Nakos, G./ Kanavaros, P.


ARDS pathophysiology is characterized by complex mechanisms that involve cells of inflammation, lung tissue cells, cytokines, chemokines, as well as apoptosis activators and inhibitors. There are two important theories that link apoptosis with ARDS and suggest that epithelial cell apoptosis, as well as the accumulation of neutrophils in the lung, may contribute to a cascade of events and, finally, ARDS. The activation of the Fas/FasL pathway is an important mechanism of alveolar epithelial injury in the lungs of patients with ALI. In addition, neutrophilic inflammation in the alveolar spaces is characteristic of ALI in humans and in most animal models of ALI. The enhanced phagocytosis of apoptotic neutrophils could lead to resolution of inflammation and repair during ARDS. In this review, we will focus on elucidating the role of apoptosis in the pathophysiology of ARDS and the contribution of Fas-mediated inflammation in ARDS. Furthermore, we will give evidence that TNF-alpha, IL-1beta and IL-13 attenuate the pro-cell death effects of Fas/CD95 on A549 epithelial cells, at least partially, by the NF-kB and PI3-K pathways, suggesting that induction of the expression of antiapoptotic genes protects the epithelial cells from cell death. (c) 2009 Elsevier GmbH. All rights reserved.
Institution and School/Department of submitter: Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας
Keywords: acute respiratory distress syndrome,apoptosis,epithelial cells,neutrophils,acute lung injury,colony-stimulating factor,nf-kappa-b,artery endothelial-cells,fas/fas ligand system,human fas ligand,neutrophil apoptosis,epithelial-cells,mediated cytotoxicity,extracellular atp
URI: http://olympias.lib.uoi.gr/jspui/handle/123456789/9691
ISSN: 0344-0338
Link: <Go to ISI>://000276208100001
http://ac.els-cdn.com/S0344033809002982/1-s2.0-S0344033809002982-main.pdf?_tid=4d00a1a471f02014928c4ddf4642287a&acdnat=1333033637_a79c14aeaf8d8ca49e0b58324d45079b
Publisher: Elsevier
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά)

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