Literature DB >> 17988850

Evaluation of bronchoalveolar lavage fluid from ARDS patients with regard to apoptosis.

Keu Sung Lee1, Young Hwa Choi, Young Sun Kim, Seung Hee Baik, Yoon Jung Oh, Seung Soo Sheen, Joo Hun Park, Sung Chul Hwang, Kwang Joo Park.   

Abstract

BACKGROUND: Apoptosis is thought to play an important role in the development of acute respiratory distress syndrome (ARDS). We evaluated the bronchoalveolar lavage (BAL) fluid from ARDS patients focusing on apoptosis.
METHODS: The study enrolled 31 ARDS patients and 20 healthy controls. BAL fluid levels of caspase-cleaved cytokeratin-18 (CK-18) and soluble mediators such as interleukin-8 (IL-8), soluble Fas (sFas), soluble Fas ligand (sFasL), growth-related oncogene-alpha (GRO-alpha), granulocyte colony-stimulating factor (G-CSF), and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) were measured using enzyme-linked immunosorbent assay (ELISA).
RESULTS: The BAL fluid caspase-cleaved CK-18 levels in ARDS patients were higher than those in controls, reflecting increased epithelial apoptosis, and were correlated with lung injury scores (rs=0.49). The BAL fluid levels of all mediators were significantly higher in ARDS patients than in controls. In ARDS patients, the BAL fluid IL-8 level was positively correlated with the levels of sFas (rs=0.57), GRO-alpha (rs=0.47), and TRAIL (rs=0.45). The BAL fluid IL-8 (rs=0.61), sFas (rs=0.57), G-CSF (rs=0.44), and TRAIL (rs=0.33) levels were correlated with the BAL fluid neutrophil count. The G-CSF levels were significantly higher in non-surviving than in surviving ARDS patients [median 183.4 pg/mL (interquartile range 76.7-315.9) vs. 63.8 pg/mL (36.2-137.2); p<0.05]. The sFas levels were positively correlated with the PaO2/FiO2 ratio (rs=0.40), and the TRAIL levels were negatively correlated with the multiple organ dysfunction scores (rs=-0.37).
CONCLUSIONS: Among the mediators in BAL fluid from ARDS patients, G-CSF had the most significant prognostic implications, and the sFas and TRAIL levels were correlated with clinical severity.

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Year:  2007        PMID: 17988850     DOI: 10.1016/j.rmed.2007.10.001

Source DB:  PubMed          Journal:  Respir Med        ISSN: 0954-6111            Impact factor:   3.415


  28 in total

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Journal:  J Immunol       Date:  2010-03-03       Impact factor: 5.422

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Authors:  Alex W Farnand; Alison J Eastman; Raquel Herrero; Josiah F Hanson; Steve Mongovin; William A Altemeier; Gustavo Matute-Bello
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6.  Therapeutic accessibility of caspase-mediated cell death as a key pathomechanism in indirect acute lung injury.

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7.  NOX1 is responsible for cell death through STAT3 activation in hyperoxia and is associated with the pathogenesis of acute respiratory distress syndrome.

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Journal:  Int J Clin Exp Pathol       Date:  2014-01-15

8.  Differential role of the Fas/Fas ligand apoptotic pathway in inflammation and lung fibrosis associated with reovirus 1/L-induced bronchiolitis obliterans organizing pneumonia and acute respiratory distress syndrome.

Authors:  Andrea D Lopez; Sreedevi Avasarala; Suman Grewal; Anuradha K Murali; Lucille London
Journal:  J Immunol       Date:  2009-12-15       Impact factor: 5.422

9.  p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment.

Authors:  Jamie A Saxon; Dong-Sheng Cheng; Wei Han; Vasiliy V Polosukhin; Allyson G McLoed; Bradley W Richmond; Linda A Gleaves; Harikrishna Tanjore; Taylor P Sherrill; Whitney Barham; Fiona E Yull; Timothy S Blackwell
Journal:  J Immunol       Date:  2016-01-15       Impact factor: 5.422

Review 10.  Gene Therapy for Acute Respiratory Distress Syndrome.

Authors:  Jing Liu; David A Dean
Journal:  Front Physiol       Date:  2022-01-17       Impact factor: 4.566

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