Effects of soluble TNF receptor treatment on lipopolysaccharide-induced myocardial cytokine expression
| Autor: | Arthur M. Feldman, Paul D. Robbins, Carole S. Frye, Simon C. Watkins, Toshiaki Kadokami, Charles F. McTiernan, Toru Kubota, George S. Bounoutas |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Lipopolysaccharides
Male Chemokine Lipopolysaccharide Physiology medicine.medical_treatment Recombinant Fusion Proteins Gene Expression Receptors Tumor Necrosis Factor Adenoviridae Pathogenesis chemistry.chemical_compound Mice Antigens CD Physiology (medical) medicine Animals RNA Messenger Interleukin 6 Receptor Chemokine CCL2 Mice Knockout biology Septic shock Interleukin-6 Tumor Necrosis Factor-alpha Myocardium medicine.disease Immunohistochemistry Interleukin-12 Shock Septic Recombinant Proteins Interleukin-10 Mice Inbred C57BL Cytokine chemistry Solubility Receptors Tumor Necrosis Factor Type I Immunology biology.protein Cytokines Tumor necrosis factor alpha Cardiology and Cardiovascular Medicine Interleukin-1 |
| Zdroj: | American journal of physiology. Heart and circulatory physiology. 280(5) |
| ISSN: | 0363-6135 |
| Popis: | Tumor necrosis factor (TNF)-α plays a key role in the pathogenesis of septic shock syndrome, and myocardial TNF-α expression may contribute to this pathophysiology. We examined the myocardial expression of TNF-α-related cytokines and chemokines in mice exposed to lipopolysaccharide (LPS) and tested the effects of anti-TNF therapy on myocardial cytokine expression. Cytokine mRNA levels were measured by RNase protection assay, and protein levels in the plasma and myocardium were assessed by enzyme-linked immunosorbent assays. LPS (4 μg/g body wt ip) induced marked cytokine expression, including TNF-α, interleukin (IL)-1β, IL-6, and monocyte chemotactic protein (MCP)-1, in both the plasma and myocardium. Pretreatment with adenovirus-mediated TNF receptor fusion protein (AdTNFR1; 109plaque-forming units iv) decreased plasma cytokine levels. In contrast, whereas myocardial IL-1β expression was also suppressed, expression of IL-6 and MCP-1 was not inhibited by AdTNFR1. In summary, anti-TNF treatment differentially altered the cytokine expression in the plasma and myocardium during endotoxemia. Inability to block myocardial expression of IL-6 and MCP-1 suggests a possible mechanism for the failure of anti-TNF therapies in the treatment of endotoxin shock. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|