scholarly journals Cytokine Synthesis by Chondroblastoma: Relation to Local Inflammation

2009 ◽  
Vol 17 (1) ◽  
pp. 56-61 ◽  
Author(s):  
C Uchikawa ◽  
T Shinozaki ◽  
T Nakajima ◽  
K Takagishi
Keyword(s):  
Tumour Necrosis ◽  
Cytokine Production ◽  
Giant Cell Tumour ◽  
Prostaglandin E ◽  
Local Inflammation ◽  
Tnf Α ◽  
Cytokine Synthesis ◽  
Joint Arthritis ◽  
Necrosis Factor ◽  
Immunohistochemical Analyses

Purpose. To investigate cytokine production by chondroblastoma in inducing local inflammation and adjacent-joint arthritis. Methods. Immunohistochemical analyses of curetted tissues using anti-human interleukin (IL)-1β, IL-6, IL-8, and tumour necrosis factor (TNF)-α were performed for 6 patients with chondroblastoma and 3 patients with giant cell tumour (GCT) of bone. In addition, prostaglandin E2, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, and TNF-α in the cyst fluid of one of the patients with chondroblastoma and 2 with GCT of bone were measured using immunoassay kits. Conclusion. Cytokines such as IL-1β, IL-8, TNF-α, and particularly IL-6 play an important role in local inflammation in patients with chondroblastoma.

scholarly journals Shiga Toxin-Induced Tumor Necrosis Factor Alpha Expression: Requirement for Toxin Enzymatic Activity and Monocyte Protein Kinase C and Protein Tyrosine Kinases

2000 ◽  
Vol 68 (9) ◽  
pp. 5183-5189 ◽  
Author(s):  
Gregory H. Foster ◽  
Cassandra S. Armstrong ◽  
Ramesh Sakiri ◽  
Vernon L. Tesh
Keyword(s):  
Shiga Toxin ◽  
Tumor Necrosis ◽  
Kinase Inhibitors ◽  
Cytokine Production ◽  
Necrosis Factor Alpha ◽  
Kinase C ◽  
Tnf Α ◽  
Factor Alpha ◽  
Cytokine Synthesis ◽  
Necrosis Factor

ABSTRACT Infections with Shiga toxin (Stx)-producing bacteria cause bloody diarrhea which may progress to life-threatening complications, including acute renal failure and neurological abnormalities. The precise mechanism of disease progression is unclear, although evidence suggests that the localized production of the host proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin-1 may exacerbate toxin-mediated vascular damage. Purified Stxs have been demonstrated to elicit proinflammatory cytokine synthesis from human peripheral blood mononuclear cells and monocytic cell lines in vitro. To understand toxin-monocyte interactions required for cytokine synthesis, we have treated differentiated THP-1 cells with purified wild-type toxins, enzymatic mutants, or B subunits and measured TNF-α production. Our data suggest that A subunit enzymatic activity is essential for cytokine production. THP-1 cells were treated with a series of protein kinase C (PKC), PKA, and protein tyrosine kinase inhibitors to examine the role of intracellular signaling molecules in Stx-mediated cytokine production. Treatment of cells with PKC and tyrosine kinase inhibitors blocked TNF-α secretion by Stx-stimulated THP-1 cells. Stx treatment directly activated PKC, which occurred at a point upstream of transcriptional activation of the gene encoding TNF-α.

scholarly journals Carrageenan-induced acute inflammation in the mouse air pouch synovial model. Role of tumour necrosis factor

1997 ◽  
Vol 6 (1) ◽  
pp. 32-38 ◽  
Author(s):  
M. Romano ◽  
R. Faggioni ◽  
M. Sironi ◽  
S. Sacco ◽  
B. Echtenacher ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Prostaglandin E ◽  
Local Inflammation ◽  
Air Pouch ◽  
Necrosis Factor

We used the mouse air pouch model of inflammation to study the interaction between cytokines, prostaglandin E2(PGE2) and cell migration during the various phases of acute local inflammation induced by carrageenan. In serum, the levels of interleukin 1 (IL-1), interleukin 6 (IL-6), tumour necrosis factor (TNF), serum amiloid-A (SAA) and Fe++were never different from controls, indicating that no systemic inflammatory changes were induced. Locally the exudate volume and the number of leukocytes recruited into the pouch increased progressively until 7 days after carrageenan. The same was true for PGE2production. We could not measure IL-1 but the production of IL-6 and TNF reached a maximum after 5-24 h then quickly decreased. Anti-TNF antibodies inhibited cell migration by 50% 24 h after treatment. Pretreatment with interleukin 10 (IL-10) inhibited TNF production almost completely and cell migration by 60%. Carrageenan-induced inflammation was modulated by anti-inflammatory drugs. Pretreatment with dexamethasone (DEX) or indomethacin (INDO) inhibited cell migration and reduced the concentration of TNF in the exudate. Production of PGE2or vascular permeability did not correlate with the number of cells in the pouch. Local TNF seems to play an important role in this model, particularly for leukocyte migration in the first phase of the inflammatory process. In conclusion, the air pouch seems to be a good model for studying the regulation of the early events of local inflammation, particularly the role of cytokines and cell migration.

scholarly journals Cytokine profile after rubella vaccine inoculation: evidence of the immunosuppressive effect of vaccination

2003 ◽  
Vol 12 (4) ◽  
pp. 203-207 ◽  
Author(s):  
Alexander L. Pukhalsky ◽  
Galina V. Shmarina ◽  
Maria S. Bliacher ◽  
Irina M. Fedorova ◽  
Anna P. Toptygina ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Cytokine Production ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tumour Necrosis Factor Α ◽  
Lymphocyte Response ◽  
Rubella Vaccine ◽  
Live Virus ◽  
Factor Α ◽  
Necrosis Factor

Background:Immunization with live virus vaccines may cause an immunosuppression with lymphopaenia, impaired cytokine production and defective lymphocyte response to mitogenes. These abnormalities were described in subjects vaccinated against measles. This study was performed to analyse the host immune response related to immunosuppression in subjects vaccinated with live attenuated rubella vaccine.Methods:Eighteen schoolgirls, aged 11-13 years, were vaccinated with live attenuated rubella vaccine Rudivax®. Before immunization, and 7 and 30 days after, peripheral blood was collected. Cellular fractions were subjected to flow cytometric analysis, and the lymphocyte response to phytohaemagglutinin was investigated. Plasma samples were analysed for cytokines (interleukin (IL)-4, IL-10, tumour necrosis factor-α, and interferon-γ) by enzyme-linked immunosorbent assay techniques.Results:On day 7 after vaccination, the number of each lymphocyte subset was decreased; however, only for CD3 and CD4 lymphocytes has a significant reduction been shown. On the contrary, tumour necrosis factor-α and IL-10 levels markedly increased and amounted to its maximum on day 30. Simultaneously, a significant reduction in plasma interferon-γand a profound decrease of the lymphocyte response to phytohaemagglutinin were shown. The changes were accompanied with marked elevation of plasma IL-4.Conclusions:Our data indicate that the vaccination with live attenuated rubella vaccine results in moderate but sustained immune disturbance. The signs of immunosuppression, including defective lymphocyte response to mitogene and impaired cytokine production, may persist for at least 1 month after vaccination.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

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