scholarly journals Passive immunization of mice against D factor blocks lethality and cytokine release during endotoxemia.

1993 ◽  
Vol 178 (3) ◽  
pp. 1085-1090 ◽  
Author(s):  
M I Block ◽  
M Berg ◽  
M J McNamara ◽  
J A Norton ◽  
D L Fraker ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Intraperitoneal Administration ◽  
Passive Immunization ◽  
Serum Levels ◽  
Acute Injury ◽  
Cytokine Release ◽  
Inflammatory Conditions ◽  
Inflammatory Cytokine Response ◽  
The Many ◽  
Necrosis Factor

D factor, also known as leukemia inhibitory factor, is a pleiotropic cytokine whose role during acute injury and inflammation is not known. Intraperitoneal administration of Escherichia coli endotoxin induced D factor gene expression in mice, and passive immunization against D factor protected them from the lethal effects of endotoxin and blocked endotoxin-induced increases in serum levels of interleukin 1 and 6. Peak levels of tumor necrosis factor and interferon gamma were not affected. These results indicate that D factor is an essential early mediator of the inflammatory cytokine response and therefore may be important in the pathogenesis of the many inflammatory conditions, such as sepsis, arthritis, allograft rejection, and cancer immunotherapy.

scholarly journals Intraperitoneal Administration of Rosuvastatin Prevents Postoperative Peritoneal Adhesions by Decreasing the Release of Tumor Necrosis Factor

2018 ◽  
Vol 91 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Stefan Chiorescu ◽  
Octavian Aurel Andercou ◽  
Nicolae Ovidiu Grad ◽  
Ion Aurel Mironiuc
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Intraperitoneal Administration ◽  
Serum Levels ◽  
Control Group ◽  
Peritoneal Adhesions ◽  
Group I ◽  
Anti Inflammatory ◽  
Necrosis Factor

Objectives. The purpose of this experimental study was to demonstrate the reduction of peritoneal adhesions formation in rats after intraperitoneal administration of rosuvastatin, due to its anti-inflammatory effect.Method. Peritoneal adhesions were induced in 120 Wistar-Bratislava rats divided into 4 groups (n=30), using a parietal and visceral (cecal) abrasion model. Group I was designated as control group; in group II, a saline solution was administered intraperitoneally; in groups III and IV, a single dose of rosuvastatin solution, 10 mg/kg and 5 mg/kg respectively, was injected intraperitoneally. The serum values of tumor necrosis factor (TNF-α) and interleukin-1 (IL-1α) were determined on day 1 and day 7 postoperatively (ELISA). Macroscopic assessment of the peritoneal adhesions was conducted on day 14.Results. Rosuvastatin therapy induced a significant decrease of tumor necrosis factor serum levels in groups III and IV, on day 1 and day 7 (p<0.01). Intraperitoneal administration of rosuvastatin correlated with a decrease of mean interleukin-1α levels on postoperative day 1 in groups III (p=0.0013) and IV (p=0.00011), but not on day 7, where the differences were no longer statistically significant (p=0.8) The reduction of postoperative peritoneal adhesions in the experimental rat model is supported by the anti-inflammatory effect of rosuvastatin, mediated mainly by the tumor necrosis factor.Conclusions. Rosuvastatin prevents the formation of postoperative peritoneal adhesions in rats. This effect may be linked to the inhibition of proinflammatory cytokines release in the early stages of adhesions formation. The present study suggests that rosuvastatin may be an efficient pharmacological agent in the prevention of postoperative peritoneal adhesions development, and requires further studies as it has a promising application value.

scholarly journals Signal transduction in host cells by a glycosylphosphatidylinositol toxin of malaria parasites.

1993 ◽  
Vol 177 (1) ◽  
pp. 145-153 ◽  
Author(s):  
L Schofield ◽  
F Hackett
Keyword(s):  
Signal Transduction ◽  
Interleukin 1 ◽  
Host Cells ◽  
Rational Basis ◽  
Cytokine Release ◽  
Cytokine Induction ◽  
Kinase C ◽  
Pathogenic Process ◽  
Necrosis Factor

In this study, we have identified a dominant glycolipid toxin of Plasmodium falciparum. It is a glycosylphosphatidylinositol (GPI). The parasite GPI moiety, free or associated with protein, induces tumor necrosis factor and interleukin 1 production by macrophages and regulates glucose metabolism in adipocytes. Deacylation with specific phospholipases abolishes cytokine induction, as do inhibitors of protein kinase C. When administered to mice in vivo the parasite GPI induces cytokine release, a transient pyrexia, and hypoglycemia. When administered with sensitizing agents it can elicit a profound and lethal cachexia. Thus, the GPI of Plasmodium is a potent glycolipid toxin that may be responsible for a novel pathogenic process, exerting pleiotropic effects on a variety of host cells by substituting for the endogenous GPI-based second messenger/signal transduction pathways. Antibody to the GPI inhibits these toxic activities, suggesting a rational basis for the development of an antiglycolipid vaccine against malaria.

Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways

2007 ◽  
Author(s):  
Valerie M. Wolfe ◽  
Seonghun Park ◽  
Marjana Tomic ◽  
Peter A. Torzilli ◽  
C. T. Christopher Chen
Keyword(s):  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Interleukin 1 ◽  
Tensile Load ◽  
Cartilage Degradation ◽  
Acute Injury ◽  
Cyclic Compression ◽  
Tnf Α ◽  
Necrosis Factor ◽  
Pro Inflammatory Cytokines

Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.

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