Abstract
Clinical trials with anti-inflammatory agents in patients with sepsis are based on the assumption that excessive proinflammatory activity of the cytokine network negatively influences the outcome of severe bacterial infections. The failure of these trials to show clinical benefit, in conjunction with recent experimental data, raises doubt about the validity of this assumption. This article reevaluates the role of cytokines in the pathogenesis of sepsis and severe bacterial infections. The cytokine network is discussed as consisting of proinflammatory cytokines, antiinflammatory cytokines, and soluble inhibitors of proinflammatory cytokines.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Bacterial Infections / drug therapy
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Bacterial Infections / etiology*
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Bacterial Infections / microbiology
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Cytotoxins / blood
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Cytotoxins / pharmacology
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Cytotoxins / physiology*
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ErbB Receptors / blood
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ErbB Receptors / metabolism
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ErbB Receptors / therapeutic use
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Humans
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Interferon-gamma / physiology
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Interleukin 1 Receptor Antagonist Protein
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Interleukin-1 / physiology
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Interleukin-10 / antagonists & inhibitors
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Interleukin-10 / physiology
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Interleukin-12 / physiology
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Interleukin-6 / pharmacology
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Interleukin-6 / physiology
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Receptors, Interleukin-1 / blood
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Receptors, Interleukin-1 / metabolism
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Receptors, Tumor Necrosis Factor / metabolism
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Sepsis / drug therapy
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Sepsis / etiology*
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Sepsis / microbiology
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Sialoglycoproteins / pharmacology
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Sialoglycoproteins / therapeutic use
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Tumor Necrosis Factor-alpha / physiology
Substances
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Cytotoxins
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IL1RN protein, human
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Interleukin 1 Receptor Antagonist Protein
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Interleukin-1
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Interleukin-6
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Receptors, Interleukin-1
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Receptors, Tumor Necrosis Factor
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Sialoglycoproteins
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Tumor Necrosis Factor-alpha
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Interleukin-10
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Interleukin-12
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Interferon-gamma
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ErbB Receptors