Induction by Toxic-Shock-Syndrome Toxin-1 of a Circulating Tumor Necrosis Factor-Like Substance in Rabbits and of Immunoreactive Tumor Necrosis Factor and Interleukin-1 from Human Mononuclear Cells

Ikejima, Takashi; Okusawa, Seijiro; Meer, J.W.M. van der; Dinarello, Charles A.

doi:10.1093/infdis/158.5.1017

Cited by 94 publications

(42 citation statements)

References 30 publications

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“…Soluble stimuli such as LPS, phytohemagglutinin, and toxic shock syndrome toxin-1 induce nearly equal amounts of IL-l1a, IL-1/, and TNF (5-15 ng/ml) with somewhat more IL-la produced by most donors (35,36). Particulate stimuli such as Staphylococcus epidermidis induce threefold more IL-1O than However, there appears to be more IL-1ra than IL-1: synthesized by PBMC using various stimuli (37).…”

Section: Resultsmentioning

confidence: 99%

Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist.

Miller

Isa²,

Vannier³

et al. 1992

J. Clin. Invest.

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Lyme arthritis is one of the few forms of chronic arthritis in which the cause is known with certainty. Because cytokines are thought to contribute to the pathogenesis of chronic arthritis, we investigated the effect of the Lyme disease spirochete, Borrelia burgdorferi, on the gene expression and synthesis of IL-1,8 and the IL-1 receptor antagonist (IL-lra) in human peripheral blood mononuclear cells. Live B. burgdorferi induced fivefold more IL-1l@ than IL-la and sevenfold more IL-1l8 than IL-lra; LPS or sonicated B. burgdorferi induced similar amounts of all three cytokines. This preferential induction of IL-1,B was most dramatic in response to a low passage, virulent preparation of B. burgdorferi vs. three high passage avirulent strains. No difference in induction of IL-lra was seen between these strains. The marked induction of IL-1iB was partially diminished by heat-treatment and abrogated by sonication; ILlra was not affected. This suggested that a membrane component(s) accounted for the preferential induction of IL-1i6. However, recombinant outer surface protein ,B induced little IL-1i6. burgdorferi-induced IL-1A6 mRNA showed biphasic elevations at 3 and 18 h. B. burgdorferi-induced IL-lra mRNA peaked at 12 h, whereas LPS-induced IL-lra mRNA peaked at 9 h. 8 synthesis increased in response to increasing numbers of spirochetes, whereas IL-lra synthesis did not. The preferential induction by B. burgdorferi of IL-1i8 over IL-lra is an example of excess agonist over antagonist synthesis induced by a microbial pathogen, and may contribute to the destructive lesion of Lyme arthritis. (J. Clin. Invest. 1992. 90:906-912.)

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Section: Resultsmentioning

confidence: 99%

Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist.

Miller

Isa²,

Vannier³

et al. 1992

J. Clin. Invest.

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“…It was essential to exclude a significant contribution of these products to the prophylactic effect observed in our model, because endotoxin [7][8][9][10][11][12][13] and several staphylococcal exotoxins [33][34][35] are potent in vitro and in vivo inducers of TNF production and release. Although the staphylococcal strain used to prepare prophylactic components was an active producer of both a-toxin [30] and TSST-l (unpublished data), neither ofthese exotoxins nor endotoxin could be demonstrated in our preparations of prophylactically active components.…”

Section: Discussionmentioning

confidence: 99%

Contribution of Tumor Necrosis Factor to Host Defense against Staphylococci in a Guinea Pig Model of Foreign Body Infections

Vaudaux¹,

Ge²,

Huggler³

et al. 1992

Journal of Infectious Diseases

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“…Heat-killed S. epidermidis, heat-killed E. coli, LTA, and LPS were compared for their ability to induce the production of TNF and IL-I in vitro. Rabbit PBMC were isolated by Ficoll-Hypaque centrifugation as previously described (26) ,gg/ml ofpolymyxin B (PMB, clinical grade; Pfizer, Inc., New York) for 1 hr at room temperature, then added to PBMC to block the effect of LPS. LTA was prepared from S. epidermidis and characterized by previously published procedures (28,29).…”

Section: Methodsmentioning

confidence: 99%

“…LTA was prepared from S. epidermidis and characterized by previously published procedures (28,29). Total TNF and IL-I production by PBMC were determined after three cycles offreeze-thawing, as previously described (26).…”

Section: Methodsmentioning

confidence: 99%

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Staphylococcus epidermidis induces complement activation, tumor necrosis factor and interleukin-1, a shock-like state and tissue injury in rabbits without endotoxemia. Comparison to Escherichia coli.

Wakabayashi¹,

Gelfand²,

Jung³

et al. 1991

J. Clin. Invest.

233

140

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IntroductionTumor necrosis factor (TNF) and IL-I are thought to mediate many of the pathophysiologic changes of endotoxemia and Gram-negative bacteremia. In these studies, heat-killed Staphylococcus epidermidis were infused into rabbits to determine whether an endotoxin (LPS)-free microorganism also elicits cytokinemia and the physiologic abnormalities seen in Gramnegative bacteremia. S. epidermidis induced complement activation, circulating TNF and IL-1, and hypotension to the same degree as did one-twentieth the number of heat-killed Escherichia coli. Circulating IL-1ft levels had a greater correlation coefficient (r = 0.81, P < 0.001) with the degree of hypotension than TNF levels (r = 0.48, P < 0.02). Leukopenia, thrombocytopenia, diffuse pulmonary capillary aggregation of neutrophils, and hepatic necrosis with neutrophil infiltration were observed to the same extent after either S. epidermidis or E. coli infusion. However, S. epidermidis infusion did not induce significant (< 60 pg/ml) endotoxemia, whereas E. coli infusion resulted in high (11,000 pg/ml) serum endotoxin levels. S. epidermidis, E. coli, LPS, or S. epidermidis-derived lipoteichoic acid (LTA) induced TNF and IL-1 from blood mononuclear cells in vitro. E. coli organisms and LPS were at least 100-fold more potent than S. epidermidis or LTA. Thus, a shock-like state with similar levels of complement activation as well as circulating levels of IL-1 and TNF were observed following either S. epidermidis or E. coli. These data provide further evidence that host factors such as IL-1 and TNF are common mediators ofthe septic shock syndrome regardless ofthe organism. (J. Clin. Invest. 1991. 87:1925-1935

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Induction by Toxic-Shock-Syndrome Toxin-1 of a Circulating Tumor Necrosis Factor-Like Substance in Rabbits and of Immunoreactive Tumor Necrosis Factor and Interleukin-1 from Human Mononuclear Cells

Cited by 94 publications

References 30 publications

Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist.

Live Borrelia burgdorferi preferentially activate interleukin-1 beta gene expression and protein synthesis over the interleukin-1 receptor antagonist.

Contribution of Tumor Necrosis Factor to Host Defense against Staphylococci in a Guinea Pig Model of Foreign Body Infections

Staphylococcus epidermidis induces complement activation, tumor necrosis factor and interleukin-1, a shock-like state and tissue injury in rabbits without endotoxemia. Comparison to Escherichia coli.

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