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At least 775 records · Page 43Linked to original sources
PubMed2006

Different ratios of eicosapentaenoic and docosahexaenoic omega-3 fatty acids in commercial fish oils differentially alter pro-inflammatory cytokines in peritoneal macrophages from C57BL/6 female mice.

The use of fish oil (FO) as a dietary supplement to prevent or reduce the severity of cardiovascular diseases and autoimmune disorders such as rheumatoid arthritis is receiving much attention. Several recent reports indicate that eating fish often or the use of small doses of FO capsules appears to have benefits against cardiovascular diseases. We have reported in the past that diets enriched with FO protect against renal diseases and prolong the life span of autoimmune-prone mice compared to corn oil (CO) diets. However, the optimum ratio of eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) in commercially available FOs to reduce the production of various pro-inflammatory cytokines has not been well established. We, therefore, obtained deodorized FO from three sources containing different EPA/DHA contents, fed them to C57BL/6 mice for 8 weeks in a 10% (vol/wt) diet (oil A, 11/10; oil B, 14/9; oil C, 23/14) and compared them with (10%) CO-fed mice as control. TNF-alpha, IL-6 and IL-1beta were measured by enzyme-linked immunosorbent assay in thioglycollate-induced macrophages, 8 and 24 h after lipopolysaccharide treatment. The results showed a significant decrease in TNF-alpha after only 8 h in oil C. After 24 h, TNF-alpha, IL-6 and IL-1beta levels decreased only in mice fed oil C, although nonsignificant decreases were seen in mice fed oil A compared to mice fed CO. The antioxidant enzymes, catalase and glutathione transferase, were higher in kidneys of mice fed oil C compared to mice fed CO. The study suggests that anti-inflammatory activity may vary among different sources of FO due to variations in EPA/DHA content.

Animals↗
PubMed2004

Lignification and structural biomass production in tobacco with suppressed caffeic/5-hydroxy ferulic acid-O-methyl transferase activity under ambient and elevated CO concentrations.

To investigate the relationship between growth, biomass partitioning and lignification we used tobacco (Nicotiana tabacum) in which O-methyl transferase (OMT) activity, an enzyme involved in the pathway of sinapyl alcohol formation for lignin synthesis, was suppressed by antisense transformation. To modulate growth, controls and transformed tobacco plants were grown under ambient (approximately 380 p.p.m) or elevated CO(2) (700 p.p.m), respectively. Lignin concentrations and composition were determined with spectrophotometric methods (thioglycolate and acetyl bromide) and Fourier transform infrared (FTIR) spectroscopy, respectively. A comparison of the thioglycolate and acetylbromide method suggested that the thioglycolate method was sensitive to changes in the syringyl/guaiacyl (S/G)-ratio in lignin and therefore not suitable for quantification in tissues with altered lignin composition. Growth under elevated CO(2) increased leaf and stem biomass of both genotypes by 40 and 20%, respectively, compared with ambient CO(2) and had no effect on root biomass. OMT suppression did not affect lignin concentrations in the leaves but caused a shift in biomass partitioning from the structural to the non-structural fraction. Elevated CO(2) caused a shift towards production of structural compounds resulting in decreased foliar lignin concentrations and indicating that the lignin/structural mass ratio is flexible in leaves. By contrast, the lignin concentrations of stems were unaffected by elevated CO(2) or OMT suppression and increased about three-fold from the apex to the base. Antisense-OMT plants produced more stem biomass than controls but showed no changes of the relative partitioning of biomass to the different pools. This indicates that the metabolic control of carbon fluxes to the production of structural versus non-structural fractions is tighter in stems than in leaves. FTIR spectroscopy indicated a relative increase in guaiacyl- as compared with syringyl-units in antisense-OMT tobacco, which was more pronounced under elevated as compared with ambient CO(2). Since there was no evidence for decreased lignin concentrations in the antisense-OMT plants but increased biomass formation we suggest that less methylated lignins are 'cheaper' in biosynthetic carbon and energy demand and, thus, may enable plants to allocate increased resources to growth.

Journal Article↗
PubMed1997

Intraportal mercaptoacetate infusion increases afferent activity in the common hepatic vagus branch of the rat.

Because dissection of the common hepatic vagus branch attenuated the feeding response to intraperitoneal injection of mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in rats fed a fat-enriched diet (18% fat), the effect of MA on the discharge rate in afferents of the common hepatic vagus branch was investigated. Intraportal infusion of the Na salt of MA (200, 400, and 800 mumol/kg) in rats adapted to the 18% fat diet dose dependently increased the discharge rate in afferents of the common hepatic vagus branch, whereas NaCl and the Na salt of the structurally related compound 2-mercaptopropionate had no effect. The lowest dose of MA yielding a significant increase in the discharge rate was 400 mumol/kg. This agrees with the dose dependence of the feeding response to MA. These findings are consistent with the notion that hepatic fatty acid oxidation controls food intake by modulating the discharge rate of vagal afferents.

Acclimatization↗
PubMed1999

Dietary omega-3 polyunsaturated fatty acids reduce IFN-gamma receptor expression in mice.

Enrichment of immune cells in vivo or in vitro with omega-3 polyunsaturated fatty acid (n-3 PUFA) has been reported to diminish their response to interferon-y (IFN-gamma). We hypothesized that the n-3 PUFA-induced hyporesponsiveness to IFN-gamma is mediated, in part, by a reduction in the number of IFN-gamma receptors (IFNGR) expressed on the surface of these cells. To test this hypothesis, we fed mice experimental diets containing low or high amounts of n-3 PUFA. Thioglycollate-elicited peritoneal macrophages (PEC) were collected and tested for binding and internalization of [125I]-labeled recombinant murine IFN-gamma. High n-3 PUFA intake was associated with a significant (n = 2, p < 0.01) reduction in [125I]-IFN-gamma binding without affecting binding affinity (Kd). When studies were performed at 37 degrees C, high n-3 PUFA intake reduced internalization of [125I]-rmIFN-gamma by 20%-30% (n = 2,p < 0.001). Results from flow cytometric analysis of IFNGR-1 expression on the surface of murine splenocytes were in agreement with the binding studies. Further, total cellular IFNGR-1 from PEC and splenocytes was examined via immunoprecipitation and Western blotting. High n-3 PUFA diet was associated with a 50% decline (n = 3-6, p < 0.05) in total IFNGR-1 in both immune cell populations studied. These data suggest that reduced IFNGR expression may be responsible for immune cell hyporesponsiveness to IFN-gamma, which may, in part, explain some of the immunomodulatory and anti-inflammatory effects associated with the consumption of diets high in n-3 PUFA.

Animals↗
PubMed1975

Microspectrophotometric estimates of non-histone proteins in cell nuclei displaying differing degrees of chromatin condensation.

Nuclei isolated from mouse thymus, kidney, and liver were fixed in ethanol-acetic acetic acid; treated with dilute acid to extract histones; stained by three protein end-group procedures; and measured by scanning, integrating microspectrophotometry. Measurements were also made of nuclei isolated from the same organs and stained by the Feulgen procedure for DNA. Protein end-group procedures included pH 2.8 Biebrich scarlet (for basic groups), mercury orange (for sulfhydryl groups), and mercury orange after thioglycolate reduction (for the sum of sulfhydryl and disulfide groups). With the exception of the comparison between Feulgen-stained 2C liver and kidney nuclei, the integrated extinction values obtained for nuclei of a given organ differed significantly from the measurements of nuclei from other organs, regardless of the staining procedure. Furthermore, the integrated extinction values for 2C nuclei were highest in larger, more vesicular nuclei (from liver and kidney) and lowest in condensed thymocyte nuclei, except in the case of measurements of the disulfide content of the nuclei. In this instance, the values of integrated extinction were highest in condensed thymocyte nuclei, intermediate in kidney nuclei, and lowest in 2C liver nuclei. When 2C, 4C, and 8C liver nuclei were compared, the integrated extinction values of 4C nuclei were found to be approximately twice those of 2C nuclei whose disulfide and Feulgen values were, respectively, higher and lower than expected. The greater disulfide values and reduced Feulgen values obtained in thymocyte and 8C liver nuclei might be related to a greater degree of chromatin condensation in these nuclei, and therefore, to a reduction or selective restriction of their RNA transcriptional capacities.

Animals↗
PubMed1996

Preexposure of mouse peritoneal macrophages to lipopolysaccharide and other stimuli enhances the nitric oxide response to secondary stimuli.

The aim of this study was to compare the regulation of the production of tumor necrosis factor-alpha (TNF-alpha) and secondary nitric oxide (NO) in macrophages submitted to a sequence of two stimulations. Pre-exposure for 18 h of mouse thioglycollate-elicited peritoneal macrophages to low doses (1-10 ng/ml) of lipopolysaccharide (LPS), in the presence or absence of serum, induces on one hand a desensitization (endotoxin tolerance) for secondary TNF-alpha responses to LPS and, on the other hand, a 4 fold increase (priming) of secondary NO responses. Preexposure to components from Gram-positive bacteria (lipoteichoic acid, peptidoglycan) and to a synthetic lipid structurally related to lipid A (compound M4), induced similar effects. In contrast to the desensitization for TNF-alpha secretion, the priming for NO production was not mimicked by sodium nitroprusside, a generator of NO. The results suggest that concomitant but distinct activation pathways induced by LPS and other agents can be dissociated by serum-independent modulation processes elicited by pre-exposure of the cells to LPS itself, or to other stimuli.

Animals↗
PubMedDate not supplied

Stability of SM-7338, a new carbapenem in mediums recommended for the susceptibility testing of anaerobic bacteria and gonococci.

The stability of SM-7338 was compared to that of imipenem in media used for susceptibility testing anaerobic bacteria and Neisseria gonorrhoeae. SM-7338 was more stable in all media than imipenem. For tests with anaerobic bacteria, the broth-disk elution (in thioglycolate) and other methods recommended by the National Committee for Clinical Laboratory Standards can be accurately used for SM-7338. However, the cysteine content of IsoVitaleX (25.9 g/L) supplement inactivates SM-7338 (20-fold reduction) in gonococcal susceptibility test systems with GC agar base. A cysteine-free supplement would be advised for tests with the carbapenems and clavulanic acid. The SM-7338 disk diffusion test (10 micrograms) results were not significantly influenced by the inactivating substances in the media.

Bacteria, Anaerobic↗
PubMed1980

Degradation of connective tissue matrices by macrophages. I. Proteolysis of elastin, glycoproteins, and collagen by proteinases isolated from macrophages.

We have investigated the ability of neutral and lysosomal enzymes of mouse macrophages to degrade the insoluble extracellular matrices secreted by smooth muscle cells, endothelial cells, and fibroblasts. Matrices produced by smooth muscle cells contained glycoproteins, elastin, and collagens, but matrices of endothelial cells and fibroblasts contained no elastin. Sequential enzyme digestion of residual matrix revealed that plasmin, a product of macrophage plasminogen activation, degraded 50-70% of the glycoprotein in the matrices but did not degrade the elastin or the collagens. Purified macrophage elastase degraded glycoprotein and elastin components but had no effect on the collagens. The rate of elastin degradation by macrophage elastase was decreased in the presence of the glycoproteins. In contrast, human granulocyte elastase effectively degraded the matrix glycoproteins, elastin, and, to a lesser extent, collagens, Mammalian collagenase degraded only collagens. Conditioned medium from resident and inflammatory macrophages, containing mixtures of the secreted proteinases, degraded the glycoprotein and elastin components of the matrices. However, conditioned medium was less effective in degrading matrix than comparable amounts of purified macrophage elastase because > 90% of the elastase in the medium was in a latent form. Inclusion of plasminogen in the assays accelerated degradation. In the presence of plasminogen, glycoproteins were degraded readily by medium from P388D1, pyran copolymer-, thioglycollate-, and periodate-elicited macrophages and, to a lesser extent, by medium from endotoxin-elicited and resident macrophages; medium from P388D1, thioglycollate-, and periodate-elicited macrophages was most effective in elastin degradation, and resident, endotoxin-elicited and pyran copolymer-elicited macrophages degraded almost no elastin. The macrophage cathepsins D and B degraded all the matrix components at an optimum pH of 5.5 and acted with the secreted neutral proteinases to degrade the connective tissue macromolecules to amino acids and oligopeptides. These data indicate that macrophages at inflammatory sites contain and secrete proteolytic enzymes that could degrade the extracellular matrix.

Animals↗
PubMed1981

Release of iron by resident and stimulated mouse peritoneal macrophages following ingestion and degradation of transferrin-antitransferrin immune complexes.

A method of loading macrophages from normal and inflammatory mouse peritoneal exudates with 59Fe using 59Fe, 125I-transferrin-antitransferrin immune complexes is described and the subsequent release of iron and degraded transferrin to the incubation medium has been studied. Release of iron occurred more rapidly from resident macrophages than from thioglycollate broth-induced (stimulated) macrophages, but degradation of the 125I-transferrin in the immune complexes was faster in stimulated cells. A small percentage of the iron released was in the form of ferritin. Desferrioxamine (1 mM) increased the release of iron from both stimulated and resident macrophages, the effect being proportionally greater in the stimulated cells. Ascorbic acid (1 mM) had no effect on the release of iron, nor did the addition of apotransferrin (1 mg/ml) to the culture medium. These results support the concept of a blockade of iron release by reticuloendothelial cells in states of inflammation, and suggest that it may be a primary cause of the anaemia of chronic disease.

Animals↗
PubMed1988

Method for testing the sterility of total nutrient admixtures.

A test for determining the sterility of a total nutrient admixture (TNA) containing equal quantities of 10% fat emulsion (Liposyn II), 8.5% amino acids injection, and 50% dextrose injection using the USP membrane filtration procedure was developed and evaluated. Membrane filter selection was determined by analysis of flow rates, membrane fluid compatibility, bubble point stability, and rinse fluid requirements. Microbial challenges employing five organisms (Bacillus subtilis, Escherichia coli, Candida albicans, Staphylococcus aureus, and Pseudomonas aeruginosa) and both soybean casein digest and fluid thioglycollate media were used to confirm the ability of the test to detect low-level microbial contamination. A polyvinylidene fluoride membrane was determined to be the most appropriate of the membrane types studied because of its superior flow rate and membrane-fluid compatibility. Bubble point testing revealed no detrimental effects on the membrane. The potential problem of haziness caused by retention of the TNA by the membrane with subsequent release in the culture media (which could result in false-positive growth determinations) was diminished by using a sterile 0.1% peptone solution rinse and careful observation techniques. Performance of the sterility test by six hospital pharmacists required an average of 14.2 minutes. Sterility testing of alternate TNAs compounded with Intralipid and Nutralipid was not feasible because of prolonged filtration times. The basic USP membrane filtration procedure for large-volume injections can be used by hospital pharmacists for testing the sterility of TNAs. When fat emulsions are used in compounding, sterility-testing procedures specific to the emulsion product used should be developed and evaluated.

Culture Media↗
PubMedDate not supplied

[Isolation of Helicobacter pylori from dental plaque].

It has been suggested that oral dissemination might be the major transmission vehicle for Helicobacter pylori, and that dental plaque might act as its reservoir. The presence of H. pylori was investigated in 62 odontological male and female patients (average age: 35 years old). Samples were taken from supragingival plaque, placed in 0.3 ml of thioglycolate broth, cultured within 12 h in Mueller-Hinton agar with the addition of 5-7% of sheep blood and antibiotic supplement, and incubated at 37 degrees C in microaerophilia for 5-7 days. Typical colonies were identified by gram, urease, oxidase and catalase. H. pylori was detected in a 15 year-old patient suffering from gastric acidity (1.61% positivity index). The medium used facilitated recovery of the agent from a sample abundant in germs. H. pylori was not recovered from the same patient 12 months later, suggesting that there might have been a transitory passage by gastric reflux or that the bacterium was acquired from an exogenous source.

Adolescent↗
PubMed1992

Role of resident macrophages in canatoxin-induced in vivo neutrophil migration.

Canatoxin (Cntx), a toxic protein purified from Canavalia ensiformis seeds, was shown to have lipoxygenase-mediated effects either in vivo or in vitro. Data here show that Cntx induced a dose-dependent migration of neutrophils and mononuclear cells when injected into rat peritoneal cavities. Furthermore, Cntx was able to induce neutrophil migration into pleural cavities and into air pouches. These effects were inhibited by dexamethasone but not by inhibitors of arachidonic acid metabolism (indomethacin, NDGA, and BW-755c) or by a PAF antagonist (BN 52021). In the peritoneal cavity Cntx caused an increase in vascular permeability inhibited by dexamethasone and BW-755c. Neutrophil migration induced by this toxin was dependent on the number of resident macrophages, since the migratory effect was enhanced by increasing the peritoneal macrophage population with thioglycollate pretreatment and was diminished when this population was reduced by peritoneal wash. It was also observed that Cntx induced release of a chemotactic factor from macrophage monolayers in vitro. Dexamethasone blocked this release but did not affect in vivo neutrophil recruitment induced by that factor. These data suggest that Cntx-induced neutrophil migration may be mediated by the same macrophage-derived neutrophil chemotactic factor released by other stimuli such as LPS, IL-1, and INF-gamma.

Animals↗
PubMedDate not supplied

Use of dithiodiglycolic acid as a tether for cationic lipids decreases the cytotoxicity and increases transgene expression of plasmid DNA in vitro.

Two major barriers that limit cationic lipids in gene delivery are low transfection efficiency and toxicity. In the present studies, we used dithiodiglycolic acid as a new tether for the polar and hydrophobic domains of a cationic lipid, cholesteryl hemidithiodiglycolyl tris(aminoethyl)amine (CHDTAEA). We compared the transfection activity and toxicity of CHDTAEA with its nondisulfide analogue and cholesteryl N-(dimethylaminoethyl) carbamate (DC-Chol). The liposomes of CHDTAEA had more than 2 orders of magnitude greater transfection activity than DC-Chol in CHO cells and 7 times greater transfection activity in SKnSH cells. CHDTAEA also demonstrated much less toxicity than the other two lipids. Dithiodiglycolic acid may act as an excellent linker in the application of cationic lipid syntheses.

Animals↗
PubMed1994

Purification and Properties of Cystathionine [gamma]-Synthase from Wheat (Triticum aestivum L.).

Cysthathionine [gamma]-synthase (CS), an enzyme involved in methionine biosynthesis, was purified from an acetone powder prepared from wheat (Triticum aestivum L.). After several chromatographic steps and radiolabeling of the partially purified enzyme with sodium cyanoboro[3H]hydride, a single polypeptide with a molecular weight of 34,500 was isolated by sodium dodecyl sulfate-high performance electrophoresis chromatography. Since the molecular weight of the native enzyme was 155,000, CS apparently consists of four identical subunits. The pyridoxal 5[prime]-phosphate-dependent forward reaction has a pH optimum of 7.5 and follows a hybrid ping-pong mechanism with Km values of 3.6 mM and 0.5 mM for L-homoserine phosphate and L-cysteine, respectively. L-Cysteine methyl ester, thioglycolate methyl ester, and sodium sulfide were also utilized as thiol substrates. The latter observation suggests that CS and phosphohomoserine sulfhydrase might be a single enzyme. CS does not seem to be a regulatory enzyme but was irreversibly inhibited by DL-propargylglycine (Ki = 45 [mu]M, Kinact = 0.16 min-1). Furthermore, the homoserine phosphate analogs 4-(phosphonomethyl)-pyridine-2-carboxylic acid, Z-3-(2-phosphonoethen-1-yl)pyridine-2-carboxylic acid, and DL-E-2-amino-5-phosphono-3-pentenoic acid acted as reversible competitive inhibitors with Ki values of 45, 40, and 1.1 [mu]M, respectively.

Journal Article↗
PubMed2004

Intracellular and cell surface localization of a complex between alphaMbeta2 integrin and promatrix metalloproteinase-9 progelatinase in neutrophils.

We have recently demonstrated that promatrix metalloproteinases (proMMPs), particularly proMMP-9, are potent ligands of the leukocyte beta(2) integrins. We studied here the complex formation between proMMP-9 and alpha(M)beta(2), the major MMP and integrin of neutrophils. On resting neutrophils, the proMMP-9/alpha(M)beta(2) complex was primarily detected in intracellular granules, but after cellular activation it became localized to the cell surface, as demonstrated by immunoprecipitation and double immunofluorescence. Further indication of the complex formation was that neutrophils and alpha(M)beta(2)-transfected L cells, but not the wild-type L cells or leukocyte adhesion deficiency cells, bound to immobilized proMMP-9 or its recombinant catalytic domain in a beta(2) integrin-dependent manner. Peptides that bound to the alpha(M) integrin-I domain and inhibited its complex formation with proMMP-9 prevented neutrophil migration in a transendothelial assay in vitro and in a thioglycolate-elicited peritonitis in vivo. These results suggest that the translocating proMMP-9/alpha(M)beta(2) complex may be part of the cell surface machinery guiding neutrophil migration.

Amino Acid Sequence↗
PubMed2002

Inflammation and cancer, the mastocytoma P815 tumor model revisited: triggering of macrophage activation in vivo with pro-tumorigenic consequences.

Subcutaneous in vivo injections of cells of the mastocytoma line P815 in syngenic DBA/2 mice induce locally fast growing solid tumors. These have been used extensively as a cancer model to analyze and manipulate the relationship between tumor cells and host's immune defenses. We report that progression of P815 tumors in vivo was accompanied by a burst (Days 5-7) of local inflammatory cells recruitment and angiogenesis observed histologically, corroborated in vivo by MRI with gadolinium, overtranscription of macrophage activation marker genes, secretion of TNF-alpha by regional lymph node cells and concomitant systemic inflammation. No substantial overtranscriptions of either VEGF or IL-10 or TGF-beta genes were observed. Induction of COX-2 gene was a late event. To establish a possible relationship between the tumor-induced local, regional and systemic increase of pro-inflammatory mediators and progression of tumors in vivo, we carried out experiments deliberately modulating the inflammatory status of the recipient animals. Pretreatment of recipient animals by i.p. injection of thioglycolate accelerated P815 tumor growth. At the opposite, treatment of mice with either a COX-1 + COX-2 inhibitor (aspirin, 1 mg/day/mouse) or a specific COX-2 inhibitor (celecoxib, 0.13 mg/day/mouse) for 2 weeks after injection of tumor cells, significantly reduced the size and growth rate of tumors compared to control mice. Experiments carried out in vitro indicated that peritoneal macrophages from untreated animals were strongly activated by live P815 cells and by P815 membrane preparations. The tumor-induced inflammatory reaction could establish a local micro environment favoring tumor progression. The P815 tumor model might be helpful to recognize important factors controlling host/tumor relationship.

Animals↗