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10.1016/s0171-2985(11)80350-5

http://scihub22266oqcxt.onion/10.1016/s0171-2985(11)80350-5
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7687236!ä!7687236

suck abstract from ncbi


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pmid7687236      Immunobiology 1993 ; 187 (3-5): 357-71
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  • The potentiating effect of LPS on tumor necrosis factor-alpha production by influenza A virus-infected macrophages #MMPMID7687236
  • Bender A; Sprenger H; Gong JH; Henke A; Bolte G; Spengler HP; Nain M; Gemsa D
  • Immunobiology 1993[Apr]; 187 (3-5): 357-71 PMID7687236show ga
  • Infection of murine PU5-1.8 macrophages and human monocytes by influenza A virus was associated with virus replication, release of tumor necrosis factor-alpha (TNF-alpha) and subsequent cell death. In the presence of small and by itself rather inefficient concentrations of lipopolysaccharide (LPS) or free lipid A (1 to 10 ng/ml), TNF-alpha production of virus-infected macrophages was strongly potentiated. LPS-triggered and enhanced TNF-alpha release from virus-infected macrophages was neither due to increased cell survival nor altered virus replication, potentiated TNF-alpha gene transcription, release of intracellularly stored TNF-alpha or shifts in the kinetics of TNF-alpha secretion. Influenza A virus infection alone induced a massive TNF-alpha mRNA accumulation which, however, was only weakly translated into bioactive TNF-alpha protein. When these virus-primed macrophages were exposed to LPS either simultaneously or up to 4 h after infection, an efficient and high translation into TNF-alpha protein occurred. Although the LPS-induced biochemical pathways leading to an augmented TNF-alpha production by virus-infected macrophages still remains unsolved, the findings suggest that the frequently observed serious clinical complications in the course of combined influenza A virus and bacterial infections may be due, at least in part, to an excessive release of cytokines such as TNF-alpha.
  • |Animals[MESH]
  • |Cell Death[MESH]
  • |Cell Line[MESH]
  • |Dinoprostone/biosynthesis[MESH]
  • |Electrophoresis, Polyacrylamide Gel[MESH]
  • |Gene Expression[MESH]
  • |Humans[MESH]
  • |Immunoblotting[MESH]
  • |Influenza A virus/*physiology[MESH]
  • |Interferons/biosynthesis[MESH]
  • |Lipid A/immunology[MESH]
  • |Lipopolysaccharides/*immunology[MESH]
  • |Macrophages/immunology[MESH]
  • |Monocytes/immunology[MESH]
  • |RNA, Messenger/analysis[MESH]
  • |Tumor Necrosis Factor-alpha/*biosynthesis/genetics[MESH]


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