Complex Modulation of Cytokine Induction by Endotoxin and Tumour Necrosis Factor from Peritoneal Macrophages of Rats by Diets Containing Fats of Different Saturated, Monounsaturated and Polyunsaturated Fatty Acid Composition

1994 ◽  
Vol 87 (2) ◽  
pp. 173-178 ◽  
Author(s):  
P. S. Tappia ◽  
R. F. Grimble
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Olive Oil ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Corn Oil ◽  
Interleukin 1 ◽  
Coconut Oil ◽  
Tumour Necrosis Factor Production ◽  
Necrosis Factor

1. Responses to cytokines and other inflammatory stimuli have been shown to be enhanced by fats rich in n − 6 polyunsaturated fatty acids and suppressed by fats rich in n − 3 polyunsaturated fatty acids and oleic acid or poor in n − 6 polyunsaturated fatty acids. 2. Corn oil is rich and coconut oil, olive oil and butter are poor in n − 6 polyunsaturated fatty acids. Olive oil and butter are rich in oleic acid. Fish oil is rich in n − 3 polyunsaturated fatty acids. 3. The present study examines the effects of feeding standard chow or corn, coconut, fish and olive oils and butter for 4 and 8 weeks on subsequent cytokine production by peritoneal macrophages of rats. 4. Tumour necrosis factor production in response to a lipopolysaccharide stimulus and interleukin-1 and interleukin-6 production in response to a tumour necrosis factor challenge were studied. 5. All fats produced a small, but statistically insignificant, reduction in tumour necrosis factor production, which was greatest for olive oil at 8 weeks. 6. After 4 weeks, fish and olive oil significantly reduced interleukin-1 production. After 8 weeks, coconut oil suppressed production of the cytokine, and the inhibitory effect of fish oil was still apparent. After 8 weeks, corn and olive oil enhanced interleukin-1 production. 7. After 4 weeks of feeding, fish and olive oil enhanced interleukin-6 production. After 8 weeks, the enhancement by these fats increased, and corn oil and butter also enhanced production. Coconut oil produced no modulatory effect. 8. Only in the cases of the effect of fish and coconut oil in interleukin-1 production, corn oil on interleukin-1 and interleukin-6 production and olive oil in tumour necrosis factor production, were the effects of fats on cytokine production in concordance with their modulatory effects on responses to cytokines and other inflammatory agents in vivo.

scholarly journals Suppression of tumour necrosis factor production from mononuclear cells by a novel synthetic compound, CLX-090717

Rheumatology ◽  
2008 ◽  
Vol 48 (1) ◽  
pp. 32-38 ◽  
Author(s):  
P. F. Sumariwalla ◽  
C. D. Palmer ◽  
L. B. Pickford ◽  
M. Feldmann ◽  
B. M. J. Foxwell ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Mononuclear Cells ◽  
Synthetic Compound ◽  
Factor Production ◽  
Tumour Necrosis Factor Production ◽  
Necrosis Factor

Tumour Necrosis Factor-α and Endotoxin Induce Less Prostaglandin E2 Production from Hypothalami of Rats Fed Coconut Oil than from Hypothalami of Rats Fed Maize Oil

1990 ◽  
Vol 79 (6) ◽  
pp. 657-662 ◽  
Author(s):  
David C. Bibby ◽  
Robert F. Grimble
Keyword(s):  
Prostaglandin E2 ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Coconut Oil ◽  
Leukotriene C4 ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
C4 Production ◽  
Necrosis Factor ◽  
Maize Oil

1. The primary aim of the study was to determine whether the stimulatory effect of tumour necrosis factor-α and endotoxin on hypothalamic prostaglandin E2 production was influenced by dietary fats containing different amounts of linoleic acid. Rats received diets containing 20% (w/w) maize oil or 19% (w/w) coconut oil plus 1% (w/w) maize oil for 8 weeks. 2. A subsidiary part of the study examined the effect of tumour necrosis factor-α on the ability of the calcium ionophore A23187 to stimulate prostaglandin E2 and leukotriene C4 production by hypothalami from chow-fed rats. 3. While tumour necrosis factor-α enhanced prostaglandin E2 production in response to A23187, neither agent had an effect on leukotriene C4 production. 4. Hypothalami from rats fed maize oil exhibited increased prostaglandin E2 production in response to both pyrogens. This did not occur with hypothalami from rats fed coconut oil. 5. Coconut oil might exert its modulatory effect by bringing about a reduction in membrane phospholipid arachidonic acid content.

Influence of butter and of corn, coconut and fish oils on the effects of recombinant human tumour necrosis factor-α in rats

1993 ◽  
Vol 84 (1) ◽  
pp. 105-112 ◽  
Author(s):  
Hilda M. Mulrooney ◽  
Robert F. Grimble
Keyword(s):  
Protein Synthesis ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Coconut Oil ◽  
Complement C3 ◽  
Tumour Necrosis Factor Α ◽  
Zinc Concentrations ◽  
Factor Α ◽  
Lung And Kidney ◽  
Necrosis Factor

1. Tumour necrosis factor-α is produced in response to inflammatory stimuli. Fish oil can suppress the production and actions of cytokines. Little information is available on the effects of other fats on cytokine biology. We compared the effects of fats, with a wide range of fatty acid characteristics, on the effects of tumour necrosis factor-α on protein and zinc metabolism in rats. 2. Weanling rats were fed for 8 weeks on diets containing 10% fat in the form of corn, fish or coconut oils or butter before an intraperitoneal injection of recombinant human tumour necrosis factor-α was given. Measurements were made 24 h after the injection. 3. In rats fed corn oil, food intake was reduced by 62% and rates of protein synthesis were increased by 86, 32 and 39% in the liver, lung and kidney, respectively. Zinc concentrations increased by 23% in the liver but decreased by 10% in the kidney. Plasma caeruloplasmin and complement C3 levels increased by 25% and 28%, respectively, and plasma albumin level decreased by 24%. 4. Fish oil prevented the increase in hepatic protein synthesis and changed the response of protein synthesis in lung and kidney to a decrease. Changes in hepatic and renal zinc concentrations were prevented. The response of the plasma caeruloplasmin level was unaltered but those of the plasma complement C3 and albumin concentrations were prevented. 5. Coconut oil and butter, although similarly low in linoleic acid, differed in their modulatory effects. With the exception of the rise in the plasma complement C3 concentration, all responses were prevented or greatly inhibited in rats fed butter. In rats fed coconut oil the increase in liver protein synthesis was reduced but that in the lung and kidney was unaffected. Changes in hepatic zinc concentration were unaffected but those in renal zinc concentration were prevented. 6. Fish and coconut oils and butter reduced the intensity of anorexia caused by tumour necrosis factor-α. The extent to which fats rich in (n-3) polyunsaturates or poor in linoleic acid modulate the metabolic response to tumour necrosis factor-α depends upon additional fatty acid characteristics.

scholarly journals Interleukin-1, Tumour Necrosis Factor and Treatment of the Septic Shock Syndrome

1992 ◽  
Vol 3 (suppl b) ◽  
pp. 11-19
Author(s):  
Charles A Dinarello
Keyword(s):  
Septic Shock ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Neutralizing Antibodies ◽  
Inflammatory Diseases ◽  
Leukocyte Adhesion ◽  
Interleukin 1 ◽  
Platelet Activating Factor ◽  
Surface Receptors ◽  
Necrosis Factor

Treating the septic shock syndrome with antibodies that block only endotoxin has its limitations. Other targets for treating septic shock include neutralizing antibodies to the complement fragment C5a, platelet activating factor antagonists and blockade of endothelial cell leukocyte adhesion molecules. Specific blockade of the pro-inflammatory cytokines interleukin-1 (IL-1) or tumour necrosis factor (TNF) reduces the morbidity and mortality associated with septic shock. Moreover, blocking IL-1 and TNF likely has uses in treating diseases other than septic shock. Use of neutralizing antibodies to TNF or IL-1 receptors has reduced the consequences of infection and inflammation, including lethal outcomes in animal models. The IL-1 receptor antagonist, a naturally occurring cytokine, blocks shock and death due to Escherichia coli as well as ameliorates a variety of inflammatory diseases. Soluble TNF and IL-1 surface receptors, which bind their respective cytokines. also ameliorate disease processes. Clinical trials are presently evaluating the safety and efficacy of anticytokine therapies either alone or in combination.

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