INVITED REVIEW |
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Year : 2010 | Volume
: 1
| Issue : 1 | Page : 29-36 |
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The dual role of TNF in pulmonary edema
Guang Yang1, Jurg Hamacher2, Boris Gorshkov1, Richard White3, Supriya Sridhar1, Alexander Verin1, Trinad Chakraborty4, Rudolf Lucas1
1 Vascular Biology Center & Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, GA, 30912, USA 2 Pulmonary Division, University Hospital, University of Bern, Bern, Switzerland 3 Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, GA, USA 4 Institute of Medical Microbiology, Justus-Liebig University of Giessen, Giessen, Germany
Correspondence Address:
Rudolf Lucas Vascular Biology Center, Medical College of Georgia, Augusta, GA,30912 USA
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PMID: 21188088
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Pulmonary edema, a major manifestation of left ventricular heart failure, renal insufficiency, shock, diffuse alveolar damage and lung hypersensitivity states, is a significant medical problem worldwide and can be life-threatening. The proinflammatory cytokine tumor necrosis factor (TNF) has been shown to contribute to the pathogenesis and development of pulmonary edema. However, some recent studies have demonstrated surprisingly that TNF can also promote alveolar fluid reabsorption in vivo and in vitro. This protective effect of the cytokine is mediated by the lectin-like domain of the cytokine, which is spatially distinct from the TNF receptor binding sites. The TIP peptide, a synthetic mimic of the lectinlike domain of TNF, can significantly increase alveolar fluid clearance and improve lung compliance in pulmonary edema models. In this review, we will discuss the dual role of TNF in pulmonary edema.
Abbreviations:-tumor necrosis factor (TNF); acute lung injury (ALI); acute respiratory distress syndrome (ARDS); positive end-expiratory pressure (PEEP);epithelial sodium channel (ENaC);neural precursor cell-expressed developmentally downregulated (gene 4) protein (Nedd4-2);serum and glucocorticoid dependent kinase (Sgk-1);insulin-like growth factor 1 (IGF-1);Protein Kinase C (PKC);reactive oxygen species (ROS);myosin light chain (MLC);pneumolysin (PLY);listeriolysin (LLO);interleukin (IL);bronchoalveolar lavage fluids (BALF);Bacillus Calmette-Guerin (BCG);TNF receptor type 1 (TNFR1); TNF receptor type 2 (TNF-R2);
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