Differential regulation of lipopolysaccharide-induced interleukin 1 and tumor necrosis factor synthesis: effects of endogenous and exogenous glucocorticoids and the role of the pituitary-adrenal axis

1989 ◽  
Vol 19 (2) ◽  
pp. 301-305 ◽  
Author(s):  
Steven H. Zuckerman ◽  
James Shellhaas ◽  
Larry D. Butter
1988 ◽  
Vol 9 (5) ◽  
pp. 72-74 ◽  
Author(s):  
Klaus Bendtzen ◽  
Åse Krogh Rasmussen ◽  
Karine Bech ◽  
Ulla Feldt-Rasmussen ◽  
Karsten Buschard

1997 ◽  
Vol 106 (8) ◽  
pp. 633-639 ◽  
Author(s):  
Jiri Prazma ◽  
Rudolph J. Triana ◽  
Steven S. Ball ◽  
C. G. Dean Dais ◽  
Harold C. Pillsbury

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.


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

1988 ◽  
Vol 167 (5) ◽  
pp. 1708-1712 ◽  
Author(s):  
R Bertini ◽  
M Bianchi ◽  
P Ghezzi

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).


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