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
• Cell Line MeSH
• Chemokines immunology   MeSH
• Cytokines immunology   MeSH
• Francisella tularensis immunology   MeSH
• Macrophages immunology   microbiology   MeSH
• Mice MeSH
• Tularemia immunology   microbiology   MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Chemokines MeSH
• Cytokines 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
• Acetylcysteine pharmacology   MeSH
• Chlorella enzymology   metabolism   radiation effects   MeSH
• Chlorophyll metabolism   MeSH
• Dithiothreitol pharmacology   MeSH
• Phenylalanine Ammonia-Lyase metabolism   MeSH
• Glutathione pharmacology   MeSH
• Catalase metabolism   MeSH
• Ascorbic Acid pharmacology   MeSH
• Nitroprusside pharmacology   MeSH
• Nitric Oxide biosynthesis   MeSH
• Oxidative Stress drug effects   physiology   MeSH
• Superoxide Dismutase metabolism   MeSH
• Ultraviolet Rays adverse effects   MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Acetylcysteine MeSH
• Chlorophyll MeSH
• Dithiothreitol MeSH
• Phenylalanine Ammonia-Lyase MeSH
• Glutathione MeSH
• Catalase MeSH
• Ascorbic Acid MeSH
• Nitroprusside MeSH
• Nitric Oxide MeSH
• Superoxide Dismutase 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
• Macrophage Activation drug effects   physiology   MeSH
• Cyclic AMP metabolism   MeSH
• Anti-Inflammatory Agents pharmacology   MeSH
• Dexamethasone pharmacology   MeSH
• Bucladesine pharmacology   MeSH
• Nucleic Acid Hybridization MeSH
• Interferon-gamma pharmacology   MeSH
• Interleukin-10 biosynthesis   MeSH
• Interleukin-12 biosynthesis   MeSH
• Lipopolysaccharides pharmacology   MeSH
• Mice, Inbred BALB C MeSH
• Mice MeSH
• Blotting, Northern MeSH
• Nitric Oxide biosynthesis   MeSH
• Macrophages, Peritoneal drug effects   enzymology   metabolism   MeSH
• RNA chemistry   genetics   MeSH
• Nitric Oxide Synthase Type II MeSH
• Nitric Oxide Synthase genetics   metabolism   MeSH
• Blotting, Western MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Cyclic AMP MeSH
• Anti-Inflammatory Agents MeSH
• Dexamethasone MeSH
• Bucladesine MeSH
• Interferon-gamma MeSH
• Interleukin-10 MeSH
• Interleukin-12 MeSH
• Lipopolysaccharides MeSH
• Nos2 protein, mouse MeSH Browser
• Nitric Oxide MeSH
• RNA MeSH
• Nitric Oxide Synthase Type II MeSH
• Nitric Oxide Synthase MeSH