Role of Complement, Interleukin-1 and Tumor Necrosis Factor in a Local Shwartzman-Like Reaction

2015 ◽  
pp. 69-78 ◽  
Author(s):  
Henry Z. Movat ◽  
Clement E. Burrowes ◽  
Myron I. Cybulsky ◽  
Charles A. Dinarello
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor

Pathogenic role of interleukin 1 and tumor necrosis factor in autoimmune endocrine diseases

1988 ◽  
Vol 9 (5) ◽  
pp. 72-74 ◽  
Author(s):  
Klaus Bendtzen ◽  
Åse Krogh Rasmussen ◽  
Karine Bech ◽  
Ulla Feldt-Rasmussen ◽  
Karsten Buschard
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pathogenic Role ◽  
Endocrine Diseases ◽  
Necrosis Factor

Role of Tumor Necrosis Factor and Interleukin-1 in Endotoxin-Induced Middle Ear Effusions

1997 ◽  
Vol 106 (8) ◽  
pp. 633-639 ◽  
Author(s):  
Jiri Prazma ◽  
Rudolph J. Triana ◽  
Steven S. Ball ◽  
C. G. Dean Dais ◽  
Harold C. Pillsbury
Keyword(s):  
Tumor Necrosis Factor ◽  
Middle Ear ◽  
Rat Model ◽  
Tumor Necrosis ◽  
Otitis Media With Effusion ◽  
Interleukin 1 ◽  
Enzyme Linked Immunosorbent Assay ◽  
Novel Approach ◽  
Necrosis Factor

In a rat model, we investigated the role of tumor necrosis factor (TNF) and interleukin-1 (IL-1) in endotoxin-induced middle ear effusions (MEEs). After the eustachian tube was obstructed, the middle ear was transtympanically injected with 35μL of either 1) 1 mg/ mL lipopolysaccharide (LPS); 2) LPS and 100 μg TNF binding protein (TNFbp); 3) LPS and 1 μg IL-1 receptor antagonist (IL-1ra); or 4) LPS, TNFbp, and IL-1ra. Every 2 hours, the fluid within the middle ear was collected, and the quantity of albumin in the fluid, an index of vascular leakage, was determined by enzyme-linked immunosorbent assay. After 6 hours, the middle ear was fixed for histologic analysis. The TNFbp significantly attenuated vascular extravasation into the middle ear. The IL-1ra did not significantly alter effusion development. These results indicate that TNF, but not IL-1, is a mediator of LPS-induced MEE. Therefore, TNFbp may represent a novel approach to the treatment of otitis media with effusion.

scholarly journals Adrenalectomy sensitizes mice to the lethal effects of interleukin 1 and tumor necrosis factor.

1988 ◽  
Vol 167 (5) ◽  
pp. 1708-1712 ◽  
Author(s):  
R Bertini ◽  
M Bianchi ◽  
P Ghezzi
Keyword(s):  
Tumor Necrosis Factor ◽  
Effective Dose ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Endotoxic Shock ◽  
Minimal Effective Dose ◽  
Lethal Effects ◽  
Necrosis Factor

To clarify the possible role of TNF and IL-1 in endotoxic shock, the lethality of rTNF (human and murine) and IL-1 in adrenalectomized mice was studied. Adrenalectomy, which has long been known to increase the susceptibility to endotoxin, rendered mice susceptible to TNF and IL-1 in terms of mortality. The lethality of endotoxin, TNF, or IL-1 was totally prevented by pretreatment with dexamethasone (minimal effective dose, 0.3 mg/Kg) but not by ibuprofen (10 mg/Kg).

Differential effects of interleukin-1 and tumor necrosis factor on ketogenesis

1992 ◽  
Vol 263 (2) ◽  
pp. E301-E309 ◽  
Author(s):  
R. A. Memon ◽  
K. R. Feingold ◽  
A. H. Moser ◽  
W. Doerrler ◽  
S. Adi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Inhibitory Effect ◽  
Acid Oxidation ◽  
Serum Free Fatty Acids ◽  
Malonyl Coa ◽  
Necrosis Factor

To determine the role of cytokines in mediating the decrease in ketones associated with infection, we studied the effect of endotoxin (LPS), interleukin-1 (IL-1), and tumor necrosis factor (TNF) on serum and hepatic ketone body levels (KB), serum free fatty acids (FFA), and hepatic malonyl-CoA levels. LPS decreased serum and hepatic KB in C57Bl/6 (LPS sensitive) mice, whereas it had little effect in C3H/HeJ (LPS resistant) mice, whose macrophages lack the ability to produce IL-1 and TNF in response to LPS, suggesting that IL-1 and TNF may mediate this effect. IL-1 and TNF decreased serum KB in both strains of mice. As seen with LPS, IL-1 decreased hepatic KB, whereas TNF had no such effect. LPS, IL-1, and TNF increased hepatic malonyl-CoA levels. TNF acutely raised serum FFA, whereas LPS and IL-1 did not. Postulating that the TNF-induced increase in FFA overrides the inhibitory effect of malonyl-CoA on fatty acid oxidation and ketogenesis, we used R-2-phenylisopropyladenosine to block TNF-induced lipolysis and demonstrated that in the absence of increased fatty acid flux, TNF inhibits KB formation. As seen with LPS, IL-1, but not TNF, decreased KB in the fasting state. These data suggest that IL-1 and TNF may mediate the antiketogenic effect of infection and that IL-1 has properties closest to that of LPS.

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