Nitric oxide (NO) stimulated the activity of plasma membrane H+-ATPase, 5'-nucleotidase, peroxidase, ascorbate peroxidase and glutathione reductase in ultraviolet B (UV-B) irradiated Chlorella pyrenoidosa. It also boosted the activity of nitrogen-metabolism enzymes such as nitrate reductase, nitrite reductase, glutamine synthetase, which were inhibited by UV-B irradiation. The chlorophyll fluorescence ratio (Fv/Fm) of the UV-B irradiated algae and decreased continuously after the cells were transferred to UV-B irradiation. A continuing decrease of the Fv/Fm was observed even after the cells were transferred to photosynthetically active radiation (PAR). After adaptation for 8 h under PAR (after treatment with nitric oxide), Fv/Fm recovered to 55 % of normal levels--without NO the value approached zero. Exogenous NO stopped the decay of chlorophyll and thylakoid membrane in cells exposed to UV-B irradiation. NO plays probably a key role in damage induced by UV-B irradiation in green algae.

• MeSH
• Algal Proteins metabolism   MeSH
• Cell Membrane enzymology   MeSH
• Chlorella physiology   radiation effects   MeSH
• Enzymes metabolism   MeSH
• Nitric Oxide physiology   MeSH
• Second Messenger Systems * MeSH
• Ultraviolet Rays * MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Algal Proteins MeSH
• Enzymes MeSH
• Nitric Oxide MeSH

Immunoprotective potential of delivered lipopolysaccharide (LPS) preparation from Klebsiella pneumoniae was determined in a murine model of lobar pneumonia. Protection was assessed with three doses of LPS (25, 50 and 100 microg; without any adjuvant) administered intranasally or intramuscularly. After evaluation of lung tissue (bacterial load and histopathology), no significant protection was observed at 25 microg with either application. A significant decrease in lung bacterial load coupled with fall in severity of lung lesions was observed with 50 microg (again both applications). At 100 microg dose, with intramuscular route, a further decrease in the lung bacterial load was shown compared to the 50 microg dose. In contrast, 100 microg LPS, when given intranasally, resulted in a higher bacterial colonization of the lung tissue and higher lung pathology; thus we recommend intramuscular instead of the intranasal route for developing protection against K. pneumoniae-mediated pneumonia with intact LPS-based vaccines.

• MeSH
• Administration, Intranasal MeSH
• Pneumonia, Bacterial microbiology   prevention & control   MeSH
• Immunization * MeSH
• Klebsiella Infections microbiology   prevention & control   MeSH
• Injections, Intramuscular MeSH
• Klebsiella pneumoniae growth & development   immunology   MeSH
• Lipopolysaccharides administration & dosage   immunology   isolation & purification   MeSH
• Disease Models, Animal MeSH
• Mice, Inbred BALB C MeSH
• Mice MeSH
• Lung microbiology   pathology   MeSH
• Colony Count, Microbial MeSH
• Animals MeSH
• Check Tag
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Geographicals
• India MeSH
• Names of Substances
• Lipopolysaccharides MeSH

The pig amnion was in vivo intraamniotically infected with E. coli for 10 h at 80-85 d of gestation either with the nonpathogenic O86 strain or enteropathogenic O55 strain. TNF-alpha, IL-10, IL-1beta and IFN-gamma were determined in amniotic fluids by ELISA, the expression of cytokines and some other inflammatory markers was determined by immunohistochemistry. Intraamniotic infection induced high levels of TNF-alpha in amniotic fluids which correlated with bacterial virulence whereas IL-10 was induced only by O86. The IL-1beta level did not increase significantly and was expressed in all infected membranes. IFN-gamma was negligible or absent. TNF-alpha, IL-12p40, calprotectin, HSP65 and gp91phox were found by immunohistochemistry only in amnion membranes infected with the enteropathogenic strain 055.

• MeSH
• Amnion immunology   microbiology   MeSH
• Biomarkers metabolism   MeSH
• Cytokines metabolism   MeSH
• Escherichia coli immunology   pathogenicity   MeSH
• Escherichia coli Infections immunology   microbiology   veterinary   MeSH
• Pregnancy Complications, Infectious immunology   microbiology   veterinary   MeSH
• Interferon-gamma metabolism   MeSH
• Interleukin-1 metabolism   MeSH
• Interleukin-10 metabolism   MeSH
• Swine Diseases immunology   microbiology   MeSH
• Swine MeSH
• Pregnancy MeSH
• Tumor Necrosis Factor-alpha metabolism   MeSH
• Inflammation immunology   MeSH
• Animals MeSH
• Check Tag
• Pregnancy MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Biomarkers MeSH
• Cytokines MeSH
• Interferon-gamma MeSH
• Interleukin-1 MeSH
• Interleukin-10 MeSH
• Tumor Necrosis Factor-alpha MeSH

Due to a gene defect (Lps(d)), C3H/HeJ mice are known to be hyporesponsive to the immunobiological potential of lipopolysaccharide (LPS). We studied dose requirements for LPS, IFN-gamma, and cytokines TNF-alpha and IL-10 to produce nitric oxide (NO) in peritoneal macrophages (Mphi) from these animals. In contrast to the Lps(n) C3H/HeN mice, high concentrations of LPS (up to 5 microg/mL) or IFN-gamma (up to 5 ng/mL) by themselves were unable to activate NO production in C3H/HeJ Mphi. The failure to produce NO could not be overcome by addition of L-arginine or tetrahydropterin. The high-output NO biosynthesis was dose-dependently stimulated by combined administration of varying concentrations of IFN-gamma (50-5000 pg/mL) and LPS (approximately 1 ng/mL) or to a lesser extent by IFN-gamma plus TNF-alpha or TNF-alpha/IL-10. Formation of NO in C3H/HeJ MCO triggered by high concentration of LPS (approximately 1 microg/mL) given together with IFN-gamma (0.2-5 ng/mL) reached the values typical for Lps(n) C3H/HeN mice. While Mphi from C3H/HeN mice secreted TNF-alpha, IL-10, and IL-10 upon contact with a low dose of LPS (1 ng/mL), C3H/HeJ Mphi required high concentration of LPS (5 microg/mL) to enhance the secretion of the cytokines. Yet, this dose remained ineffective to stimulate IFN-gamma in Mphi from C3H/HeJ mice. It can be presumed that one of the important factors influencing their deficient ability to form NO is a failure of Mphi to produce IFN-gamma upon LPS contact.

• MeSH
• Macrophage Activation immunology   MeSH
• Cytokines biosynthesis   immunology   metabolism   MeSH
• Escherichia coli immunology   metabolism   MeSH
• Interferon-gamma immunology   metabolism   MeSH
• Interleukin-10 immunology   metabolism   MeSH
• Lipopolysaccharides immunology   MeSH
• Mice, Inbred C3H MeSH
• Mice MeSH
• Nitric Oxide biosynthesis   MeSH
• Macrophages, Peritoneal immunology   metabolism   MeSH
• Tumor Necrosis Factor-alpha immunology   metabolism   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
• Cytokines MeSH
• Interferon-gamma MeSH
• Interleukin-10 MeSH
• Lipopolysaccharides MeSH
• Nitric Oxide MeSH
• Tumor Necrosis Factor-alpha 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