Pregled bibliografske jedinice broj: 4765
The effects of vasoactive intestinal peptide on production of tumor necrosis factor-alpha in vivo
The effects of vasoactive intestinal peptide on production of tumor necrosis factor-alpha in vivo // International Journal of Tissue Reactions / Kyoshima, J. (ur.).
Ženeva: Bioscience Editprint Inc., 1997. str. 61-62 (poster, međunarodna recenzija, sažetak, znanstveni)
CROSBI ID: 4765 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
The effects of vasoactive intestinal peptide on production of tumor necrosis factor-alpha in vivo
Autori
Čulo, Filip ; Erceg, Damir
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
International Journal of Tissue Reactions
/ Kyoshima, J. - Ženeva : Bioscience Editprint Inc., 1997, 61-62
Skup
7th Interscience World Conference on Infkammation, Antirheumatics, Analgesics, Immunomodulators
Mjesto i datum
Ženeva, Švicarska, 19.05.1997. - 21.05.1997
Vrsta sudjelovanja
Poster
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
vasoactive intestinal peptide; TNF-alpha; cAMP
Sažetak
There are increasing body of data showing that vasoactive intestinal peptide (VIP) acts as an immunomodulator and that it inhibits a variety of lymhocyte and macrophage function. It was shown that mononuclear cells have specific receptors for VIP and VIP increases the level of cAMP in these cells. Since several agents that increase cAMP level in mononuclear cells inhibit the production of tumor necrosis factor-a (TNF-a), we investigated the production of TNF-a in mice that were pretreated with VIP. The effect of VIP on TNF-a production was determined in in three different experimental models. In the first model, saline or VIP (2 ug per mouse i.p) were given to normal mice 15 minutes before they were given lipoplysaccharide (LPS) i.v. (10 ug per mouse). In the second model, the VIP or saline and LPS were given at the same doses and shedule in mice given 18 days before i.v. 1.5 mg of BCG (living bacteria, Institute Pasteur). In both models, TNF-a was determined in serum taken from mice 90 minutes after LPS injection. In the third model, mice were infected with E. coli (3x108 bacteria i.v., strain B6, Sigma) and VIP (2 mg per mouse) or saline were given i.p. 15 minutes later. The serum for TNF-a determination two and half hours after bacteria injection. In all models, TNF-a was determined in pooled sera obtained from 4-6 mice per group, by bioassay with L929 sensitive cells. In all three models, TNF-a level was 4 to 15 times lower in mice pretreated with VIP than in control mice pretreated in saline. In further experiments, we are investigating the dose- and time-response to VIP, as well as the effect of VIP on survival of mice treated as in second and third model.
Izvorni jezik
Engleski
Znanstvena područja
Farmacija
POVEZANOST RADA
Ustanove:
Medicinski fakultet, Zagreb