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Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1.

Mediators of inflammation

Tőzsér J, Benkő S.
PMID: 27672241
Mediators Inflamm. 2016;2016:5460302. doi: 10.1155/2016/5460302. Epub 2016 Sep 08.

IL-1

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Tőzsér J, Benkő S. Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1. Mediators Inflamm. 2016;2016:5460302doi: 10.1155/2016/5460302.
Tőzsér, J., & Benkő, S. (2016). Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1. Mediators of inflammation, 20165460302. https://doi.org/10.1155/2016/5460302
Tőzsér, József, and Benkő, Szilvia. "Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1." Mediators of inflammation vol. 2016 (2016): 5460302. doi: https://doi.org/10.1155/2016/5460302
Tőzsér J, Benkő S. Natural Compounds as Regulators of NLRP3 Inflammasome-Mediated IL-1. Mediators Inflamm. 2016;2016:5460302. doi: 10.1155/2016/5460302. Epub 2016 Sep 08. PMID: 27672241; PMCID: PMC5031844.
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Trans-active factors controlling the IL-2 gene in adult human T-cell subsets.

Mediators of inflammation

Mouzaki A, Zubler RH, Doucet A, Rungger D.
PMID: 18475438
Mediators Inflamm. 1992;1(1):33-7. doi: 10.1155/S0962935192000073.

IL-2 secretion in total or subsets of PHA/PMA-stimulated PBMC-derived human T-lymphocytes was monitored and found to be largely due to CD4(+)CD8(-) cells. The presence and functional state of transcription factors (TF) was assessed by protein-DNA interaction assays and functional...

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Mouzaki A, Zubler RH, Doucet A, et al. Trans-active factors controlling the IL-2 gene in adult human T-cell subsets. Mediators Inflamm. 1992;1(1):33-7doi: 10.1155/S0962935192000073.
Mouzaki, A., Zubler, R. H., Doucet, A., & Rungger, D. (1992). Trans-active factors controlling the IL-2 gene in adult human T-cell subsets. Mediators of inflammation, 1(1), 33-7. https://doi.org/10.1155/S0962935192000073
Mouzaki, A, et al. "Trans-active factors controlling the IL-2 gene in adult human T-cell subsets." Mediators of inflammation vol. 1,1 (1992): 33-7. doi: https://doi.org/10.1155/S0962935192000073
Mouzaki A, Zubler RH, Doucet A, Rungger D. Trans-active factors controlling the IL-2 gene in adult human T-cell subsets. Mediators Inflamm. 1992;1(1):33-7. doi: 10.1155/S0962935192000073. PMID: 18475438; PMCID: PMC2365322.
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Endotoxin and cytokines in patients with gastrointestinal tract perforation.

Mediators of inflammation

Endo S, Inada K, Inoue Y, Otsu T, Kasai T, Kuwata Y, Hoshi S, Yoshida M.
PMID: 18475440
Mediators Inflamm. 1992;1(1):45-8. doi: 10.1155/S0962935192000097.

Plasma levels of endotoxin and various cytokines were assessed in 70 patients with gastrointestinal tract perforation. Sepsis developed in 29 of them, and eight of these (27.6%) had on admission endotoxin levels higher than 9.8 pg ml(-1). The clinical...

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Endo S, Inada K, Inoue Y, et al. Endotoxin and cytokines in patients with gastrointestinal tract perforation. Mediators Inflamm. 1992;1(1):45-8doi: 10.1155/S0962935192000097.
Endo, S., Inada, K., Inoue, Y., Otsu, T., Kasai, T., Kuwata, Y., Hoshi, S., & Yoshida, M. (1992). Endotoxin and cytokines in patients with gastrointestinal tract perforation. Mediators of inflammation, 1(1), 45-8. https://doi.org/10.1155/S0962935192000097
Endo, S, et al. "Endotoxin and cytokines in patients with gastrointestinal tract perforation." Mediators of inflammation vol. 1,1 (1992): 45-8. doi: https://doi.org/10.1155/S0962935192000097
Endo S, Inada K, Inoue Y, Otsu T, Kasai T, Kuwata Y, Hoshi S, Yoshida M. Endotoxin and cytokines in patients with gastrointestinal tract perforation. Mediators Inflamm. 1992;1(1):45-8. doi: 10.1155/S0962935192000097. PMID: 18475440; PMCID: PMC2365315.
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Stimulation of neutrophil functions by C5a(desArg): an in vitro model of haemodialysis.

Mediators of inflammation

Eckle I, Kolb G, Martin EM, Havemann K.
PMID: 18475443
Mediators Inflamm. 1992;1(1):61-6. doi: 10.1155/S0962935192000127.

Cuprophane membranes during haemodialysis significantly increase the plasma levels of C5a(desArg) (maximal 55 mug C5a(adesArg)/1 blood after 30 min) whereas Hemophane or Polysulphonemembranes induce only low plasma levels of C5a(desArg). C5a(desArg) generated in vitro by yeast incubation of autologous...

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Eckle I, Kolb G, Martin EM, et al. Stimulation of neutrophil functions by C5a(desArg): an in vitro model of haemodialysis. Mediators Inflamm. 1992;1(1):61-6doi: 10.1155/S0962935192000127.
Eckle, I., Kolb, G., Martin, E. M., & Havemann, K. (1992). Stimulation of neutrophil functions by C5a(desArg): an in vitro model of haemodialysis. Mediators of inflammation, 1(1), 61-6. https://doi.org/10.1155/S0962935192000127
Eckle, I, et al. "Stimulation of neutrophil functions by C5a(desArg): an in vitro model of haemodialysis." Mediators of inflammation vol. 1,1 (1992): 61-6. doi: https://doi.org/10.1155/S0962935192000127
Eckle I, Kolb G, Martin EM, Havemann K. Stimulation of neutrophil functions by C5a(desArg): an in vitro model of haemodialysis. Mediators Inflamm. 1992;1(1):61-6. doi: 10.1155/S0962935192000127. PMID: 18475443; PMCID: PMC2365317.
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ICAM-1 expression on chondrocytes in rheumatoid arthritis: induction by synovial cytokines.

Mediators of inflammation

Davies ME, Sharma H, Pigott R.
PMID: 18475445
Mediators Inflamm. 1992;1(1):71-4. doi: 10.1155/S0962935192000140.

The intercellular adhesion molecule-1 (ICAM-1) was found by immunostaining chondrocytes in cartilage from three patients with rheumatoid arthritis. Expression of ICAM-1 was restricted to chondrocytes in areas of erodedcartilage adjacent to the invading synovial tissue. Toluidine blue staining of...

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Davies ME, Sharma H, Pigott R. ICAM-1 expression on chondrocytes in rheumatoid arthritis: induction by synovial cytokines. Mediators Inflamm. 1992;1(1):71-4doi: 10.1155/S0962935192000140.
Davies, M. E., Sharma, H., & Pigott, R. (1992). ICAM-1 expression on chondrocytes in rheumatoid arthritis: induction by synovial cytokines. Mediators of inflammation, 1(1), 71-4. https://doi.org/10.1155/S0962935192000140
Davies, M E, et al. "ICAM-1 expression on chondrocytes in rheumatoid arthritis: induction by synovial cytokines." Mediators of inflammation vol. 1,1 (1992): 71-4. doi: https://doi.org/10.1155/S0962935192000140
Davies ME, Sharma H, Pigott R. ICAM-1 expression on chondrocytes in rheumatoid arthritis: induction by synovial cytokines. Mediators Inflamm. 1992;1(1):71-4. doi: 10.1155/S0962935192000140. PMID: 18475445; PMCID: PMC2365319.
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Serum levels of interleukin-6 are not dependent on the kidney function.

Mediators of inflammation

Nässberger L.
PMID: 18475461
Mediators Inflamm. 1992;1(3):197-9. doi: 10.1155/S0962935192000309.

Interleukin-6, also named B-cell stimulatory factor, is a glycoprotein with a molecular weight of 26 kDa. Increased serum levels of interleukin-6 (IL-6) are found in several disease conditions. We investigated the importance of a deteriorated kidney function upon IL-6...

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Nässberger L. Serum levels of interleukin-6 are not dependent on the kidney function. Mediators Inflamm. 1992;1(3):197-9doi: 10.1155/S0962935192000309.
Nässberger, L. (1992). Serum levels of interleukin-6 are not dependent on the kidney function. Mediators of inflammation, 1(3), 197-9. https://doi.org/10.1155/S0962935192000309
Nässberger, L. "Serum levels of interleukin-6 are not dependent on the kidney function." Mediators of inflammation vol. 1,3 (1992): 197-9. doi: https://doi.org/10.1155/S0962935192000309
Nässberger L. Serum levels of interleukin-6 are not dependent on the kidney function. Mediators Inflamm. 1992;1(3):197-9. doi: 10.1155/S0962935192000309. PMID: 18475461; PMCID: PMC2365338.
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Bronchial responses to substance P after antigen challenge in the guinea-pig: in vivo and in vitro studies.

Mediators of inflammation

Boichot E, Lagente V, Gall GL, Carré C, Mencia-Huerta JM, Braquet P, Lockhart A, Frossard N.
PMID: 18475463
Mediators Inflamm. 1992;1(3):207-12. doi: 10.1155/S0962935192000322.

The effect of antigen challenge on the airway responses to substance P and on the epithelial neutral endopeptidase (NEP) activity was investigated in aerosol sensitized guinea-pigs. In vivo, bronchial responses to aerosolized substance P were similar to the responses...

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Boichot E, Lagente V, Gall GL, et al. Bronchial responses to substance P after antigen challenge in the guinea-pig: in vivo and in vitro studies. Mediators Inflamm. 1992;1(3):207-12doi: 10.1155/S0962935192000322.
Boichot, E., Lagente, V., Gall, G. L., Carré, C., Mencia-Huerta, J. M., Braquet, P., Lockhart, A., & Frossard, N. (1992). Bronchial responses to substance P after antigen challenge in the guinea-pig: in vivo and in vitro studies. Mediators of inflammation, 1(3), 207-12. https://doi.org/10.1155/S0962935192000322
Boichot, E, et al. "Bronchial responses to substance P after antigen challenge in the guinea-pig: in vivo and in vitro studies." Mediators of inflammation vol. 1,3 (1992): 207-12. doi: https://doi.org/10.1155/S0962935192000322
Boichot E, Lagente V, Gall GL, Carré C, Mencia-Huerta JM, Braquet P, Lockhart A, Frossard N. Bronchial responses to substance P after antigen challenge in the guinea-pig: in vivo and in vitro studies. Mediators Inflamm. 1992;1(3):207-12. doi: 10.1155/S0962935192000322. PMID: 18475463; PMCID: PMC2365335.
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Induction of circulating phospholipase A(2) by intravenous administration of recombinant human tumour necrosis factor.

Mediators of inflammation

Pruzanski W, Sherman ML, Kufe DW, Vadas P.
PMID: 18475466
Mediators Inflamm. 1992;1(4):235-40. doi: 10.1155/S0962935192000358.

We have examined the effects of intravenous infusion of recombinant human tumour necrosis factor (rh-TNF) on serum activity of phospholipase A(2) (PLA(2)) in patients with malignancies. Nine patients received a 24 h continuous intravenous infusion ranging from 1.0 x...

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Pruzanski W, Sherman ML, Kufe DW, et al. Induction of circulating phospholipase A(2) by intravenous administration of recombinant human tumour necrosis factor. Mediators Inflamm. 1992;1(4):235-40doi: 10.1155/S0962935192000358.
Pruzanski, W., Sherman, M. L., Kufe, D. W., & Vadas, P. (1992). Induction of circulating phospholipase A(2) by intravenous administration of recombinant human tumour necrosis factor. Mediators of inflammation, 1(4), 235-40. https://doi.org/10.1155/S0962935192000358
Pruzanski, W, et al. "Induction of circulating phospholipase A(2) by intravenous administration of recombinant human tumour necrosis factor." Mediators of inflammation vol. 1,4 (1992): 235-40. doi: https://doi.org/10.1155/S0962935192000358
Pruzanski W, Sherman ML, Kufe DW, Vadas P. Induction of circulating phospholipase A(2) by intravenous administration of recombinant human tumour necrosis factor. Mediators Inflamm. 1992;1(4):235-40. doi: 10.1155/S0962935192000358. PMID: 18475466; PMCID: PMC2365345.
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Tumour necrosis factor (TNF) and interleukin-1 (IL-1) induce muscle proteolysis through different mechanisms.

Mediators of inflammation

Zamir O, Hasselgren PO, Higashiguchi T, Frederick JA, Fischer JE.
PMID: 18475468
Mediators Inflamm. 1992;1(4):247-50. doi: 10.1155/S0962935192000371.

The purpose of this study was to test the hypothesis that muscle proteolysis induced by TNF or IL-1 is mediated by glucocorticoids. Rats were treated with 300 mug kg(-1) of recombinant human preparations of IL-1alpha (rIL-1alpha) or TNFalpha (rTNFalpha)...

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Zamir O, Hasselgren PO, Higashiguchi T, et al. Tumour necrosis factor (TNF) and interleukin-1 (IL-1) induce muscle proteolysis through different mechanisms. Mediators Inflamm. 1992;1(4):247-50doi: 10.1155/S0962935192000371.
Zamir, O., Hasselgren, P. O., Higashiguchi, T., Frederick, J. A., & Fischer, J. E. (1992). Tumour necrosis factor (TNF) and interleukin-1 (IL-1) induce muscle proteolysis through different mechanisms. Mediators of inflammation, 1(4), 247-50. https://doi.org/10.1155/S0962935192000371
Zamir, O, et al. "Tumour necrosis factor (TNF) and interleukin-1 (IL-1) induce muscle proteolysis through different mechanisms." Mediators of inflammation vol. 1,4 (1992): 247-50. doi: https://doi.org/10.1155/S0962935192000371
Zamir O, Hasselgren PO, Higashiguchi T, Frederick JA, Fischer JE. Tumour necrosis factor (TNF) and interleukin-1 (IL-1) induce muscle proteolysis through different mechanisms. Mediators Inflamm. 1992;1(4):247-50. doi: 10.1155/S0962935192000371. PMID: 18475468; PMCID: PMC2365344.
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Interleukin-6 in peripheral blood and inflammatory sites in Behçet's disease.

Mediators of inflammation

Hamzaoui K, Hamzaoui A, Kahan A, Hamza M, Chabbou A, Ayed K.
PMID: 18475474
Mediators Inflamm. 1992;1(4):281-5. doi: 10.1155/S0962935192000437.

Interleukin-6, a potent pro-inflammatory cytokine, might be involved in Behçet's disease (BD) pathological pathways. We investigated IL-6 levels in sera and synovial fluids collected from BD patients. The IL-6 production was also studied in vivo, by measuring its activity...

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Hamzaoui K, Hamzaoui A, Kahan A, et al. Interleukin-6 in peripheral blood and inflammatory sites in Behçet's disease. Mediators Inflamm. 1992;1(4):281-5doi: 10.1155/S0962935192000437.
Hamzaoui, K., Hamzaoui, A., Kahan, A., Hamza, M., Chabbou, A., & Ayed, K. (1992). Interleukin-6 in peripheral blood and inflammatory sites in Behçet's disease. Mediators of inflammation, 1(4), 281-5. https://doi.org/10.1155/S0962935192000437
Hamzaoui, K, et al. "Interleukin-6 in peripheral blood and inflammatory sites in Behçet's disease." Mediators of inflammation vol. 1,4 (1992): 281-5. doi: https://doi.org/10.1155/S0962935192000437
Hamzaoui K, Hamzaoui A, Kahan A, Hamza M, Chabbou A, Ayed K. Interleukin-6 in peripheral blood and inflammatory sites in Behçet's disease. Mediators Inflamm. 1992;1(4):281-5. doi: 10.1155/S0962935192000437. PMID: 18475474; PMCID: PMC2365351.
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Study on the pathogenesis of pathophysiological changes of burn systemic infection.

Mediators of inflammation

Ao Ngao L, Yuesheng H, Zongcheng Y.
PMID: 18475486
Mediators Inflamm. 1992;1(6):371-4. doi: 10.1155/S0962935192000553.

The present prospective study showed that incidence of systemic infection in severe burn patients was 30.9%. Toxic shock and multiple organ failure (MOF) developed in all patients with uncontrolled systemic infection. Both morbidity and mortality of MOF were 76.5%....

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Ao Ngao L, Yuesheng H, Zongcheng Y. Study on the pathogenesis of pathophysiological changes of burn systemic infection. Mediators Inflamm. 1992;1(6):371-4doi: 10.1155/S0962935192000553.
Ao Ngao, L., Yuesheng, H., & Zongcheng, Y. (1992). Study on the pathogenesis of pathophysiological changes of burn systemic infection. Mediators of inflammation, 1(6), 371-4. https://doi.org/10.1155/S0962935192000553
Ao Ngao, L, et al. "Study on the pathogenesis of pathophysiological changes of burn systemic infection." Mediators of inflammation vol. 1,6 (1992): 371-4. doi: https://doi.org/10.1155/S0962935192000553
Ao Ngao L, Yuesheng H, Zongcheng Y. Study on the pathogenesis of pathophysiological changes of burn systemic infection. Mediators Inflamm. 1992;1(6):371-4. doi: 10.1155/S0962935192000553. PMID: 18475486; PMCID: PMC2365372.
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Differential regulation of TNF-alpha and IL-1beta production from endotoxin stimulated human monocytes by phosphodiesterase inhibitors.

Mediators of inflammation

Molnar-Kimber KL, Yonno L, Heaslip RJ, Weichman BM.
PMID: 18475493
Mediators Inflamm. 1992;1(6):411-7. doi: 10.1155/S0962935192000620.

The effect of selective PDE-I (vinpocetine), PDE-III (milrinone, CI-930), PDE-IV (rolipram, nitroquazone), and PDE-V (zaprinast) isozyme inhibitors on TNF-alpha and IL-1beta production from LPS stimulated human monocytes was investigated. The PDE-IV inhibitors caused a concentration dependent inhibition of TNF-alpha...

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Molnar-Kimber KL, Yonno L, Heaslip RJ, et al. Differential regulation of TNF-alpha and IL-1beta production from endotoxin stimulated human monocytes by phosphodiesterase inhibitors. Mediators Inflamm. 1992;1(6):411-7doi: 10.1155/S0962935192000620.
Molnar-Kimber, K. L., Yonno, L., Heaslip, R. J., & Weichman, B. M. (1992). Differential regulation of TNF-alpha and IL-1beta production from endotoxin stimulated human monocytes by phosphodiesterase inhibitors. Mediators of inflammation, 1(6), 411-7. https://doi.org/10.1155/S0962935192000620
Molnar-Kimber, K L, et al. "Differential regulation of TNF-alpha and IL-1beta production from endotoxin stimulated human monocytes by phosphodiesterase inhibitors." Mediators of inflammation vol. 1,6 (1992): 411-7. doi: https://doi.org/10.1155/S0962935192000620
Molnar-Kimber KL, Yonno L, Heaslip RJ, Weichman BM. Differential regulation of TNF-alpha and IL-1beta production from endotoxin stimulated human monocytes by phosphodiesterase inhibitors. Mediators Inflamm. 1992;1(6):411-7. doi: 10.1155/S0962935192000620. PMID: 18475493; PMCID: PMC2365371.
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Showing 1 to 12 of 675 entries