Mutual interactions were investigated between intracellular parasitic bacterium Francisella tularensis (F.t.; highly virulent bacterium responsible for tularemia, replicating within the host macrophages) and murine macrophage-like cell line J774. Recombinant murine lymphokine INF-gamma and/or LPS derived from E. coli were determined to stimulate in vitro antimicrobial activity of macrophage-like J774 cell line against the live vaccine strain (LVS) of F.t. through their ability to produce proinflammatory cytokines and chemokines. F.t. infection up-regulated IL-12 p40 production and down-regulated TNF-alpha production by stimulated macrophages; on the other hand, F.t. infection did not affect the production of IL-8, IL-6, MCP-5, and RANTES by stimulated macrophages. This showed that F.t. infection modulates the cytokine synthesis by J774 macrophage cell line.

• MeSH
• buněčné linie MeSH
• chemokiny imunologie   MeSH
• cytokiny imunologie   MeSH
• Francisella tularensis imunologie   MeSH
• makrofágy imunologie   mikrobiologie   MeSH
• myši MeSH
• tularemie imunologie   mikrobiologie   MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• chemokiny MeSH
• cytokiny MeSH

The effect of ultraviolet-B radiation (UV-B; 280-320 nm) on induction of nitric oxide was estimated in the suspensions of green alga Chlorella pyrenoidosa with or without the NO scavenger N-acetyl-L-cysteine, and reductants such as 1,4-dithiothreitol, glutathione (reduced form), and ascorbic acid. Exogenously added sodium nitroprusside (NO donor), glutathione, 1,4-dithiothreitol, and ascorbic acid were able to prevent chlorophyll loss mediated by UV-B. Addition of NO to algal suspensions irradiated by UV-B increased the activity of catalase and superoxide dismutase but lowered the activity of phenylalanine ammonia-lyase. UV-B thus appears to be a strong inducer of NO production, exogenously added NO and reductants protecting the green alga against UV-B-induced oxidative damage.

• MeSH
• acetylcystein farmakologie   MeSH
• Chlorella enzymologie   metabolismus   účinky záření   MeSH
• chlorofyl metabolismus   MeSH
• dithiothreitol farmakologie   MeSH
• fenylalaninamoniaklyasa metabolismus   MeSH
• glutathion farmakologie   MeSH
• katalasa metabolismus   MeSH
• kyselina askorbová farmakologie   MeSH
• nitroprusid farmakologie   MeSH
• oxid dusnatý biosyntéza   MeSH
• oxidační stres účinky léků   fyziologie   MeSH
• superoxiddismutasa metabolismus   MeSH
• ultrafialové záření škodlivé účinky   MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• acetylcystein MeSH
• chlorofyl MeSH
• dithiothreitol MeSH
• fenylalaninamoniaklyasa MeSH
• glutathion MeSH
• katalasa MeSH
• kyselina askorbová MeSH
• nitroprusid MeSH
• oxid dusnatý MeSH
• superoxiddismutasa MeSH

The effects of cAMP-elevating agents, N6-2'-O-dibutyryl cAMP (Bu2cAMP), and glucocorticoid (dexamethasone) on the production of inflammatory mediators--nitric oxide and interleukin-12 (IL-12) and anti-inflammatory mediator interleukin-10 (IL-10) were demonstrated in murine peritoneal macrophages. Inducible nitric oxide synthase (iNOS) and iNOS mRNA were detected by northern blot and western blot, respectively. The cAMP elevating agents Bu2cAMP and prostaglandin E2 each alone did not show any effect on NO production but along with IFN-gamma and lipolysaccharide (LPS) they slightly enhanced NO production. Dexamethasone inhibited NO production in IFN-gamma- and LPS-treated cells; cAMP elevating agents interfered with the NO production inhibited by dexamethasone. Inhibition was revealed at the mRNA level as well as at protein level. Bu2cAMP or dexamethasone either alone or synergistically inhibited IL-12 production; Bu2cAMP interfered with dexamethasone-mediated inhibition of IL-10 production in IFN-gamma- and LPS-treated macrophages. The use of glucocorticoids along with cAMP elevating agents was beneficial in lowering the level of inflammatory mediator IL-12 and producing high levels of the anti-inflammatory mediator IL-10 active in cell protection. On the other hand, interference of Bu2cAMP with dexamethasone-mediated NO inhibition may have adverse effect. Therefore, adverse effects due to cAMP-mediated interference (inhibition) with NO synthesis may occur in many inflammatory diseases during combined drug therapy by glucocorticoids and cAMP elevating agents.

• MeSH
• aktivace makrofágů účinky léků   fyziologie   MeSH
• AMP cyklický metabolismus   MeSH
• antiflogistika farmakologie   MeSH
• dexamethason farmakologie   MeSH
• dibutyryl cyklický AMP farmakologie   MeSH
• hybridizace nukleových kyselin MeSH
• interferon gama farmakologie   MeSH
• interleukin-10 biosyntéza   MeSH
• interleukin-12 biosyntéza   MeSH
• lipopolysacharidy farmakologie   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• northern blotting MeSH
• oxid dusnatý biosyntéza   MeSH
• peritoneální makrofágy účinky léků   enzymologie   metabolismus   MeSH
• RNA chemie   genetika   MeSH
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého genetika   metabolismus   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• AMP cyklický MeSH
• antiflogistika MeSH
• dexamethason MeSH
• dibutyryl cyklický AMP MeSH
• interferon gama MeSH
• interleukin-10 MeSH
• interleukin-12 MeSH
• lipopolysacharidy MeSH
• Nos2 protein, mouse MeSH Prohlížeč
• oxid dusnatý MeSH
• RNA MeSH
• synthasa oxidu dusnatého, typ II MeSH
• synthasa oxidu dusnatého MeSH