Interleukin 12 Levels During the Initial Phase of Septic Shock With Purpura in Children: Relation to Severity of Disease

Hazelzet, Jan A.; Kornelisse, René F.; Kraan, Tineke C. T. M. van der Pouw; Joosten, Koen; Voort, Edwin van der; Mierlo, Gerard van; Suur, Marja H.; Hop, Wim C. J.; Groot, Ronald de; Hack, C. Erik

doi:10.1006/cyto.1997.0215

Cited by 48 publications

(33 citation statements)

References 34 publications

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“…In a different study, 29% of patients with septic shock and purpura (MCD) had elevated IFN-ã levels. These patients had signi®cantly higher IL-6, IL-8 and IL-10 but not IL-12 p40 levels, higher lactate levels and lower white blood cell counts [50]. Elevated IFN-ã levels have not been demonstrated in all studies of MCD [12] nor in adults with septic shock [24].…”

Section: Ifn-ãmentioning

confidence: 85%

“…Patients with elevated levels of p70 have signi®cantly raised IL-8. Furthermore, 29% of patients have detectable IFN-ã levels and these patients have signi®cantly raised levels of IL-6, IL-8 and IL-10 but not IL-12 p40 [50]. Whilst it has been demonstrated that IL-12 p40 levels are associated with outcome, the lack of correlation with its principal stimulant IFN-ã is dif®cult to understand.…”

Section: Il-2 Il-2 Is Mainly Produced By Activated Cd4 T Cells and Tmentioning

confidence: 99%

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Cytokines, chemokines and other effector molecules involved in meningococcal disease

Hackett

Thomson

Hart

2001

Journal of Medical Microbiology

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Section: Ifn-ãmentioning

confidence: 85%

Section: Il-2 Il-2 Is Mainly Produced By Activated Cd4 T Cells and Tmentioning

confidence: 99%

Cytokines, chemokines and other effector molecules involved in meningococcal disease

Hackett

Thomson

Hart

2001

Journal of Medical Microbiology

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“…55 p35 is constitutively transcribed, is regulated posttranslationally, 56 and is not secreted independently. In contrast, p40 production is regulated by inflammatory effectors, often to high levels, including during infection with Neisseria meningitides 57 or in autoimmune disease. 58 The lack of p40 in (ƒ, n ϭ 2); 10 7 (Ⅺ, n ϭ 3); 10 8 (F, n ϭ 3); and 10 9 (OE, n ϭ 3).…”

Section: Discussionmentioning

confidence: 99%

Sepsis and Pathophysiology of Anthrax in a Nonhuman Primate Model

Stearns-Kurosawa

Lupu

Taylor

et al. 2006

The American Journal of Pathology

103

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Studies that define natural responses to bacterial sepsis assumed new relevance after the lethal bioterrorist attacks with Bacillus anthracis (anthrax), a spore-forming, toxigenic gram-positive bacillus. Considerable effort has focused on identifying adjunctive therapeutics and vaccines to prevent future deaths, but translation of promising compounds into the clinical setting necessitates an animal model that recapitulates responses observed in humans. Here we describe a nonhuman primate (Papio c. cynocephalus) model of B. anthracis infection using infusion of toxigenic B. anthracis Sterne 34F2 bacteria (5 ؋ 10 5 to 6.5 ؋ 10 9 CFU/kg). Similar to that seen in human patients, we observed changes in vascular permeability, disseminated intravascular coagulation, and systemic inflammation. The lung was a primary target organ with serosanguinous pleural effusions, intra-alveolar edema, and hemorrhagic lesions. This animal model reveals that a fatal outcome is dominated by the host septic response, thereby providing important insights into approaches for treatment and prevention of anthrax in humans. (Am J Pathol

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“…The importance of IFN-g in host defense against intracellular pathogens has been demonstrated in several infectious disease models. Elevated levels of IFN-g have been measured in patients with sepsis and in experimental sepsis in primates [23][24][25]. Mice treated with anti-IFN-g and mice deficient in the IFN-g receptor are resistant against endotoxininduced shock [26,27].…”

Section: Discussionmentioning

confidence: 99%

Elevated Plasma Concentrations of Interferon (IFN)–γ and the IFN‐γ–Inducing Cytokines Interleukin (IL)–18, IL‐12, and IL‐15 in Severe Melioidosis

et al. 1999

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Interferon (IFN)-gamma plays an important role in the pathogenesis of sepsis. Production of IFN-gamma is stimulated by synergistic effects of interleukin (IL)-18, IL-12, and IL-15. To investigate the regulation of IFN-gamma production during severe gram-negative infection, the plasma concentrations of IFN-gamma, IL-18, IL-12, and IL-15 were measured in 83 patients with suspected melioidosis. The diagnosis was confirmed in 62 patients, 31 of whom had blood cultures positive for Burkholderia pseudomallei, of whom 12 died. Compared with healthy controls, patients had elevated levels of IFN-gamma, IL-18, IL-12p40, and IL-15 on admission, with significantly higher levels in blood culture-positive patients, and these levels remained elevated during the 72-h study period. In whole blood stimulated with heat-killed B. pseudomallei, anti-IL-12 had a stronger inhibitory effect than anti-IL-18 and anti-IL-15 on IFN-gamma production. This effect of anti-IL-12 was further enhanced by anti-IL-18. These data suggest that during gram-negative sepsis, IFN-gamma production is controlled at least in part by endogenous IL-18, IL-12, and IL-15.

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Interleukin 12 Levels During the Initial Phase of Septic Shock With Purpura in Children: Relation to Severity of Disease

Cited by 48 publications

References 34 publications

Cytokines, chemokines and other effector molecules involved in meningococcal disease

Cytokines, chemokines and other effector molecules involved in meningococcal disease

Sepsis and Pathophysiology of Anthrax in a Nonhuman Primate Model

Elevated Plasma Concentrations of Interferon (IFN)–γ and the IFN‐γ–Inducing Cytokines Interleukin (IL)–18, IL‐12, and IL‐15 in Severe Melioidosis

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