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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
1997-2-14
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pubmed:abstractText |
Inflammatory cells, in particular monocytes/macrophages, release pro-inflammatory mediators in response to several infectious and non-infectious stimuli. The excessive release of these mediators, resulting in the development of whole body inflammation, may play an important role in the pathogenesis of sepsis and septic shock. TNF-alpha, acting synergistically with cytokines such as IL-1, GM-CSF and IFN-gamma, is the key mediator in the induction process of septic shock, as shown in several experimental models. Based on this concept and on the encouraging results obtained in several experimental models, a number of clinical sepsis trials targeting the production or action of TNF-alpha or IL-1 have been performed in recent years. Unfortunately, these trials have failed to demonstrate a therapeutic benefit. One reason for this may be the lack of exact immunologic analyses during the course of septic disease. Recently, we demonstrated that there is a biphasic immunologic response in sepsis: an initial hyperinflammatory phase is followed by a hypo-inflammatory one. The latter is associated with immunodeficiency which is characterized by monocytic deactivation, which we have called "immunoparalysis". While anti-inflammatory therapy (e.g. anti-TNF antibodies, IL-1 receptor antagonist, IL-10) makes sense during the initial hyperinflammatory phase, immune stimulation by removing inhibitory factors (plasmapheresis) or the administration of monocyte activating cytokines (IFN-gamma, GM-CSF) may be more useful during "immunoparalysis".
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0342-4642
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
22 Suppl 4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S474-81
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8923092-HLA-DR Antigens,
pubmed-meshheading:8923092-Humans,
pubmed-meshheading:8923092-Immunocompromised Host,
pubmed-meshheading:8923092-Inflammation,
pubmed-meshheading:8923092-Interferon-gamma,
pubmed-meshheading:8923092-Interleukin-1,
pubmed-meshheading:8923092-Monocytes,
pubmed-meshheading:8923092-Patient Selection,
pubmed-meshheading:8923092-Prognosis,
pubmed-meshheading:8923092-Sepsis,
pubmed-meshheading:8923092-Treatment Failure,
pubmed-meshheading:8923092-Tumor Necrosis Factor-alpha
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pubmed:year |
1996
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pubmed:articleTitle |
Monocyte deactivation--rationale for a new therapeutic strategy in sepsis.
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pubmed:affiliation |
Institut für Medizinische Immunologie, Universitätsklinikum Charité, Humboldt-Universität zu Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Review
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