Source:http://linkedlifedata.com/resource/pubmed/id/12763679
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rdf:type | |
lifeskim:mentions | |
pubmed:dateCreated |
2003-5-23
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pubmed:abstractText |
In view of the increasing use of anti-cytokine-based therapies to treat autoimmune diseases, the role of specific cytokines in host defense against infection has become a highly relevant area of investigation. There are over 300,000 patients worldwide being treated with agents that specifically block the biological activities of interleukin-1 (IL-1) or tumor necrosis factor (TNF) for reducing the severity of autoimmune diseases such as rheumatoid arthritis, Crohn's disease or psoriasis. Those patients receiving anti-TNF-alpha or IL-1 blocking therapies are treated on a chronic basis. Studies suggest that other chronic inflammatory diseases will benefit from anti-cytokine therapies. However, there is a growing body of clinical evidence that neutralization of TNF-alpha is associated with an increased risk of opportunistic infections, including mycobacterial diseases. Blockade of IL-1 activity with the IL-1 receptor antagonist (IL-1Ra) appears, at present, to be relatively safe. However, because of physician under reporting (some estimates of reporting being less than 5% of these infections), the true incidence of infections, both serious and non-serious, will remain unknown. Does the increase in infections associated with anti-cytokine-based therapies come as a surprise? Of the two components of host defense, the innate and the acquired responses, which are affected by anti-cytokine therapies? From a wealth of rodent studies using live infection models, the following conclusions can be drawn: (1) neutralization or gene deletion for TNF-alpha is frequently associated with reduction of host defense in models of live Gram-positive or Gram-negative infections as well as infection by intracellular microbes such as Salmonella and Listeria; (2) absence of the IL-1 receptor can also result in decreased resistance to Listeria or Gram-positive bacteria and (3) TNF-alpha and IFN-gamma are required for defense against infection caused by Mycobacterium tuberculosis.
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pubmed:grant | |
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 |
Jun
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pubmed:issn |
0264-410X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
21 Suppl 2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
S24-34
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12763679-Animals,
pubmed-meshheading:12763679-Cytokines,
pubmed-meshheading:12763679-Disease Models, Animal,
pubmed-meshheading:12763679-Humans,
pubmed-meshheading:12763679-Infection,
pubmed-meshheading:12763679-Interferon-gamma,
pubmed-meshheading:12763679-Mice,
pubmed-meshheading:12763679-Mice, Knockout,
pubmed-meshheading:12763679-Nitric Oxide,
pubmed-meshheading:12763679-Pneumonia, Bacterial,
pubmed-meshheading:12763679-Salmonella Infections,
pubmed-meshheading:12763679-Shock, Septic,
pubmed-meshheading:12763679-Tuberculosis
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pubmed:year |
2003
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pubmed:articleTitle |
Anti-cytokine therapeutics and infections.
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pubmed:affiliation |
Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review
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