Enhanced oxidative burst without interleukin 1 production by normal human polymorphonuclear leukocytes primed with muramyl dipeptides

Inflammation ◽  
1987 ◽  
Vol 11 (2) ◽  
pp. 153-161 ◽  
Author(s):  
C. Jupin ◽  
M. Parant ◽  
L. Chedid ◽  
C. Damais
1994 ◽  
Vol 179 (2) ◽  
pp. 739-743 ◽  
Author(s):  
F Re ◽  
M Muzio ◽  
M De Rossi ◽  
N Polentarutti ◽  
J G Giri ◽  
...  

Whereas the signaling function of the interleukin 1 (IL-1) receptor type I (IL-1R I) has been well documented, the type II "receptor" has been suggested to act as a decoy target for this cytokine. Since IL-1 may represent a key target of the immunomodulatory and antiinflammatory properties of glucocorticoids (GC), the aim of this study was to investigate the effects of dexamethasone (Dex) on IL-1R expression in human polymorphonuclear leukocytes (PMN), which express predominantly the type II molecule (IL-1R II). We found that Dex augments the levels of steady state transcripts encoding the IL-1R I and, most prominently, those of IL-1R II. Dex induced both transcripts via transcription-dependent mechanisms and by prolongation of the mRNAs half-lives. Inhibition of protein synthesis superinduced basal and Dex-augmented IL-1R II mRNA, whereas it completely inhibited the induction by Dex of IL-1R I transcripts. Induction of IL-1R II mRNA by Dex was associated with augmented membrane expression and release of the type II IL-1 binding molecule. This effect was mediated by the GC receptor. Other steroids (17 beta-estradiol, progesterone, and testosterone) were ineffective. The concentrations of IL-1 alpha and IL-1 receptor antagonist required to displace the binding of IL-1 beta to the soluble form of the decoy molecule induced by Dex from PMN were, respectively, 100 and 2 times higher compared with IL-1 beta. The induction by Dex of the type II receptor, a decoy molecule for IL-1, may contribute to the immunosuppressive and antiinflammatory activities of Dex.


1984 ◽  
Vol 43 (2) ◽  
pp. 744-752 ◽  
Author(s):  
P Robinson ◽  
D Wakefield ◽  
S N Breit ◽  
J F Easter ◽  
R Penny

Blood ◽  
1976 ◽  
Vol 48 (2) ◽  
pp. 309-313 ◽  
Author(s):  
RL Baehner ◽  
LA Boxer ◽  
J Davis

Normal human polymorphonuclear leukocytes (PMN) placed in anaerobic chambers reaching pO2's of less than 5 mm Hg fail to generate O2-, iodinate ingested particles, and stimulate glucose-1–14C oxidation through the hexose monophosphate shunt. The observation that anaerobic cells are incapable of generating O2- or reducing nitroblue tetrazolium (NBT) to formazan supports the idea that NBT reduction in phagocytizing PMN is due exclusively to oxygen-dependent O2- generating oxidase which is deficient in chronic granulomatous disease leukocytes, despite their hyperphagocytic capacity.


1975 ◽  
Vol 131 (Supplement) ◽  
pp. S73-S80 ◽  
Author(s):  
K. R. Ratzan ◽  
C. Giraudo ◽  
C. Amado ◽  
I. Lauredo ◽  
G. Horowitz

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