Circulating interleukin 1 and tumor necrosis factor during inflammation

1987 ◽  
Vol 253 (6) ◽  
pp. R922-R928 ◽  
Author(s):  
L. L. Moldawer ◽  
J. Gelin ◽  
T. Schersten ◽  
K. G. Lundholm

It is proposed that interleukin 1 (IL 1) and tumor necrosis factor (TNF) alpha play central roles in the host's response to inflammation. Yet circulating concentrations have not been frequently measured in many inflammatory states. Serum levels of IL 1 and TNF were evaluated in mice with a tumor, sterile inflammation, endotoxinemia, or generalized peritonitis where an acute-phase protein response was documented. In tumor-bearing mice, no IL 1 or TNF could be detected despite marked increases in the serum concentration of the acute-phase reactant protein, amyloid P. In mice with peritonitis, induced by cecal ligation and perforation, or a turpentine-induced subcutaneous abscess, IL 1 but not TNF could be detected in the serum. Only expansion of the reticuloendothelial system with Corynebacterium parvum and subsequent challenge with endotoxin resulted in serum TNF appearance. The failure to observe IL 1 or TNF in any of the disorders could not be explained by inhibitors. Rather, the data suggest that a hepatic acute-phase protein response can occur during inflammatory states without the appearance of either IL 1 or TNF in the circulation. Circulating levels of both monokines do not appear to be a universal finding in inflammation.

1992 ◽  
Vol 1 (1) ◽  
pp. 27-31 ◽  
Author(s):  
P. Bjrök ◽  
K. Ohlsson

In this work we have focused on the ability of interleukin-1 to induce an acute phase protein response and a degranulation of polymorphonuclear leukocytes in vivo. The capacity of the interleukin-1 receptor antagonist to influence these events was also investigated. It was shown that interleukin-1 induced an acute phase protein response in rats and mice. In rats α2-macroglubolin levels were increased in plasma after an interleukin-1 injection whereas α1-inhibitor-3 decreased in plasma. In the mice plasma amyloidPwas increased. The interleukin-1 receptor antagonist blocked the increase of α2-macroglobulin and plasma amyloidPin a dose dependent way while the effect on the α1-inhibitor-3 decrease was less pronounced. Interleukin-1 led to polymorphonuclear leukocyte degranulation in vivo as measured by increased cathepsinGplasma levels. The interleukin-1 receptor antagonist could influence the early phase of this degranulation.


1990 ◽  
Vol 30 (10) ◽  
pp. 1181-1188 ◽  
Author(s):  
PAUL E. BANKEY ◽  
JOHN E. MAZUSKI ◽  
MARIAESTELA ORTIZ ◽  
JOSE M. FULCO ◽  
FRANK B. CERRA

PLoS ONE ◽  
2020 ◽  
Vol 15 (3) ◽  
pp. e0230949
Author(s):  
Arash Janmohammadi ◽  
Nariman Sheikhi ◽  
Hadi Haghbin Nazarpak ◽  
Gholamreza Nikbakht Brujeni

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