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PubMed1993

Inhibitory effect of bisbenzylisoquinoline alkaloids on nitric oxide production in activated macrophages.

Bisbenzylisoquinoline (BBI) alkaloids are anti-inflammatory constituents of plants of the families Menispermaceae and Ranunculaceae, which have been used as folk remedies in Japan and China. Five BBI alkaloids (cepharanthine, chondocurine, cycleanine, isotetrandrine and tetrandrine) were tested for suppressive effect on in vitro nitric oxide (NO) production by lipopolysaccharide-stimulated peritoneal macrophages, which were induced with thioglycollate or bacillus Calmette-Guerin in mice. All these BBI alkaloids significantly suppressed NO production at 5 micrograms/mL. Cepharanthine, isotetrandrine and cycleanine were slightly more inhibitory than tetrandrine and chondocurine. The suppression persisted for at least 48 hr. As NO is one of the critical mediators in inflammation, these results may explain some aspects of the anti-inflammatory mechanisms of BBI compounds.

Alkaloids↗

PubMed1992

Importance of the His-298 residue in the catalytic mechanism of the Streptomyces R61 extracellular DD-peptidase.

Among the active-site-serine penicillin-recognizing proteins, the Streptomyces R61 extracellular DD-peptidase is the only one to have a His-Thr-Gly sequence [instead of Lys-Thr(Ser)-Gly] in 'box' VII. The His residue was replaced by Gln or Lys. Both mutations induced a marked decrease in the rates of both tripeptide substrate hydrolysis and acylation by benzylpenicillin and cephalosporin C. The rate of hydrolysis of the thioester hippuryl thioglycollate was less affected. The most striking result was the disproportionate loss of transpeptidation properties by both mutants, indicating an important role of His-298 in this reaction. We believe that this result represents the first modification of a DD-peptidase leading to a specific decrease of the transpeptidation-to-hydrolysis ratio.

Amino Acid Sequence↗

PubMed2002

Voltammetric determination of thiodiglycolic acid in urine.

In urine the level of thiodiglycolic acid (TDGA) is a sensitive indicator of exposure of the human organism to some physiologically active or toxic substances, gases and vapors. The determination of TDGA by use of a voltammetric method based on electroreduction of TDGA in acidic solution at the hanging mercury drop electrode has been developed and practically tested. In order to eliminate the matrix effect of urine, prior to voltammetric measurement the samples are eluted from a small column of PVC powder. The method is simple, low cost, rapid and sensitive, appropriate for the needs of occupational medicine.

Electrochemistry↗

PubMedDate not supplied

[Structure and functional properties of temperature-sensitive derivatives of immobilized proteins].

Polydiethylacrylamides (degree of polymerization, 13-470) containing a terminal carboxyl group were obtained by the method of radical polymerization of N,N-diethylacrylamide in the presence of mercaptoacetic acid. In the presence of 1-ethyl-(3,3-dimethylaminopropyl)-carbodiimide, these polymers reacted with ovomucoid to produce its polymeric derivatives. The values of the lower critical mixing temperature of these derivatives and the inhibitory activities of immobilized ovomucoid were determined by the length and amount of polydiethylacrylamide macromolecules bound to the molecule of ovomucoid.

Acrylamides↗

PubMed1992

Low response of BALB/c macrophages to priming and activating signals.

Trehalose dimycolate (TDM), a mycobacterial glycolipid, is a powerful macrophage-priming agent. However, its efficiency seems limited in the case of BALB/c mice. Peritoneal macrophages harvested from TDM-treated BALB/c mice did not control BCG growth in vitro as efficiently as similar macrophages from two other mouse strains, (B6 x D2)F1 and C57BL/6, which are respectively Bcgr and Bcgs. BALB/c macrophages elicited by TDM also exhibited a low capacity to produce hydrogen peroxide and, after activation by lipopolysaccharide (LPS), weak cytostatic activity against P815 mastocytoma cells. Finally, alkaline phosphodiesterase, a marker of resident and inflammatory macrophages, was still expressed at a high level in macrophages of BALB/c mice treated with TDM. Low responsiveness of BALB/c macrophages to stimuli was not observed with TDM only; activation for tumor cytotoxicity of thioglycolate-elicited macrophages from BALB/c mice required also higher doses of interferon-gamma, and LPS. L-Arginine-dependent production of nitric oxide was inducible in macrophages from BALB/c mice, but the conditions required for its induction were more stringent. Thus, the reduced antiproliferative effects of BALB/c macrophages may be due to uncomplete induction of NO synthase after suboptimal stimulation.

Amino Acid Oxidoreductases↗

PubMed2006

Aspirin and salicylate suppress polymorphonuclear apoptosis delay mediated by proinflammatory stimuli.

During inflammation, polymorphonuclear leukocyte (PMN) apoptosis can be delayed by different proinflammatory mediators. Classically, it has been accepted that the widely used anti-inflammatory drug acetyl salicylic acid (ASA) exerts its action through inhibition of cyclooxygenases and subsequent prostaglandin synthesis. We hypothesized that another anti-inflammatory action of ASA could be the shortening of PMN survival. We found that at therapeutic concentrations (1-3 mM), ASA and its metabolite salicylate (NaSal), but not indomethacin or ibuprofen, counteracted the prolonged PMN survival mediated by lipopolysaccharide (LPS) through inhibition of nuclear factor-kappaB (NF-kappaB) activation. Both salicylates also inhibited interleukin (IL)-1alpha or acidic conditions antiapoptotic activity. Higher concentrations of both drugs had a direct apoptotic effect. Salicylates were not effective when PMN apoptosis delay was induced by granulocyte macrophage-colony-stimulating factor (GM-CSF), a NF-kappaB-independent cytokine. Promotion of PMN survival by the combination of IL-1alpha and LPS was also reversed by salicylates, but higher concentrations were required. ASA concentrations that did not trigger PMN death increase the zymosan- or tumor necrosis factor-alpha-mediated proapoptotic effect. The LPS- and IL-1alpha- but not GM-CSF-mediated antiapoptotic effect was markedly reduced in PMNs from donors who had ingested ASA. Using a thioglycolate-induced peritonitis model, we showed that in ASA- or NaSal-treated mice there was not only a decrease in the number of cells recruited but also an increase in the percentage of apoptotic PMNs as well as an enhancement of phagocytosis compared with controls. Our findings demonstrate that acceleration of PMN apoptosis by turning off the NF-kappaB-mediated survival signals elicited by proinflammatory stimuli is another anti-inflammatory action of ASA and NaSal.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1995

A chemotactic S100 peptide enhances scavenger receptor and Mac-1 expression and cholesteryl ester accumulation in murine peritoneal macrophages in vivo.

In the early development of atherosclerotic plaque, monocytes are recruited to the arterial intima where they accumulate lipid and become foam cells. The recently described murine chemotactic S100 protein, CP-10, may have an important role in this process. Intraperitoneal injection of CP-10(42-55) (chemotactic hinge region peptide) into mice caused a sustained leukocyte recruitment with a sixfold increase in monocyte numbers over 24 h. CP-10(42-55)--elicited monocyte/macrophages accumulated significantly increased cholesteryl esters in response to acetylated LDL, both in vivo and in vitro and this was associated with a twofold increase in scavenger receptor expression. By contrast, thioglycollate- and macrophage colony-stimulating factor-elicited macrophages expressed levels of scavenger receptor similar to those on resident macrophages and did not exhibit enhanced acetylated LDL loading in vitro. The leukocyte integrin Mac-1 (CD11b/CD18) and its beta subunit (CD18), but neither lymphocyte function-associated antigen-1 nor very late activation antigen-4, were upregulated on monocyte/macrophages elicited by CP-10(42-55), thioglycollate, and macrophage colony-stimulating factor. Cholesteryl ester accumulation in vitro was significantly enhanced by adhesion, which appeared to involve macrophage activation via ligation of Mac-1. The initial events of monocyte recruitment and adhesion to the vessel wall may be important in macrophage foam cell development, and CP-10 or related S100 proteins may contribute to the early inflammatory events of atherogenesis by stimulating these events.

Amino Acid Sequence↗

PubMed1983

Effects of nicotine on the fine structure of cultivated mouse peritoneal macrophages.

The effects of nicotine on the fine structure of thioglycollate-elicited mouse peritoneal macrophages cultivated in vitro was studied in order to elucidate further the mechanism behind its inhibitory effect on endocytosis and intracellular degradation of exogenous protein. In the concentrations (1.0-1,000 nM) and times (2-48 h) used here, nicotine lacked cytotoxic effect and did not appreciably affect the occurrence and distribution of different organelles. The most prominent change caused by the drug was the formation of large vacuoles believed to represent swollen lysosomes. This finding supports the idea that nicotine, like several other amines and weak bases, accumulates in the lysosomes by proton trapping. This could in turn impair the digestive capacity of the lysosomes by raising pH above the optimum of the acid hydrolases. It could also affect endocytosis and recycling of plasma membrane components. Additionally, the nicotine treatment led to an increased number of autophagic vacuoles consisting of lysosomes enclosing other lysosomes. A 'lysosomophagic' process of this type has previously been observed in other situations with decreased endocytosis. It is suggested to be a subtype of autophagy that serves the purpose of regulating the amount of lysosomes in connection with changes in the functional activity of this organelle.

Animals↗

PubMed1979

Identification of S-(carboxymethyl)-L-cysteine and thiodiglycolic acid, urinary metabolites of 2,2'-bis-(chloroethyl)-ether in the rat.

S-(carboxymethyl)-L-cysteine (CMC) and thiodiglycollic acid (TGA) were identified by gas chromatographic-mass spectrometric measurements in the urine of rats after intraperitoneal injections of 2,2'-bis-(chloroethyl)-ether (BCEE). It is therefore probable that BCEE is O-dealkylated by a mixed-function oxidation. The hepatocarcinogenic effect of BCEE may be explained by the liberation of chloroacetaldehyde in vivo.

Animals↗

PubMed1988

Enhanced oxidative mechanisms in immunologically activated versus elicited polymorphonuclear neutrophils: correlations with fungicidal activity.

Peritoneal polymorphonuclear neutrophils (PMN) from mice were tested for their ability to kill the yeast form of Blastomyces dermatitidis (Bd) in vitro and for their fungicidal mechanisms. PMN elicited from immune mice by the intraperitoneal injection of non-viable Bd (referred to as immunologically activated PMN or ActPMN) showed significantly enhanced fungicidal activity in comparison with PMN elicited with thioglycollate medium (ThioPMN) [means = 44.7% (SD 12.8%) and 16.4% (SD 9.2%) killed; n = 14; p less than 0.001]. Production of superoxide anion (O2-) by ActPMN after stimulation with phorbol myristate acetate was enhanced in comparison with production by ThioPMN. Superoxide dismutase, which removes O2-, inhibited ActPMN killing by 75% (p less than 0.001) when added to cultures immediately before challenge with Bd (optimal concentration: 6000 U/ml). Sodium azide, which inhibits myeloperoxidase and scavenges singlet oxygen (1O2), and catalase, which breaks down hydrogen peroxide (H2O2), inhibited ActPMN killing by 64% (p less than 0.001) and 52% (p less than 0.001), with optimal concentrations of 1 mM and 10,000 U/ml, respectively. Two agents that both scavenge 1O2 and antagonise hypochlorous acid (HOCl-), histidine and tryptophan, were also powerful inhibitors of ActPMN killing. Quenchers of hydroxyl radical (.OH), dimethylsulfoxide and sodium benzoate, had less effect, and required higher concentrations. These data suggest that the enhanced killing of Bd by ActPMN involves one or more oxidative mechanisms, and that there is a prominent role for O2-, either directly or as a precursor of other active oxygen species, a probable role for H2O2, and possible roles for 1O2, HOCl-, and .OH.

Animals↗

PubMed2005

Anti-inflammatory effect of heme oxygenase 1: glycosylation and nitric oxide inhibition in macrophages.

Flavonoids including the aglycones, hesperetin (HT; 5,7,3'-trihydroxy-4'-methoxy-flavanone), and naringenin (NE; 5,7,4'-trihydroxy flavanone) and glycones, hesperidin (HD; 5,7,3'-trihydroxy-4'-methoxy-flavanone 7-rhamnoglucoside) and naringin (NI; 5,7,4'-trihydroxy flavanone 7-rhamno glucoside), were used to examine the importance of rutinose at C7 on the inhibitory effects of flavonoids on lipopolysaccharide (LPS)-induced nitric oxide production in macrophages. Both HT and NE, but not their respective glycosides HD and NI, induced heme oxygenase 1 (HO-1) protein expression in the presence or absence of LPS and showed time and dose-dependent inhibition of LPS-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in RAW264.7, J774A.1, and thioglycolate-elicited peritoneal macrophages. Additive inhibitory effect of an HO-1 inducer hemin and NE or NI on LPS-induced NO production and iNOS expression was identified, and HO enzyme inhibitor tin protoporphyrin (SnPP) attenuated the inhibitory effects of HT, NE, and hemin on LPS-induced NO production. Both NE and HT showed no effect on iNOS mRNA and protein stability in RAW264.7 cells. Removal of rutinose at C7 of HD and NI by enzymatic digestion using hesperidinase (HDase) and naringinase (NIase) produce inhibitory activity on LPS-induced NO production, according to the production of the aglycones, HT and NE, by high-performance liquid chromatography (HPLC) analysis. Furthermore, the amount of NO produced by LPS or lipoteichoic acid (LTA) was significantly reduced in HO-1-overexpressing cells (HO-1/RAW264.7) compared to that in parental cells (RAW264.7). Results of the present study provide scientific evidence to suggest that rutinose at C7 is a negative moiety in flavonoid inhibition of LPS-induced NO production, and that HO-1 is involved in the inhibitory mechanism of flavonoids on LPS-induced iNOS and NO production.

Animals↗

PubMed2002

Observation of phase transition of thermo-responsive poly(NIPA)-PEI block copolymers by STM.

N-isopropylacrylamide (NIPA) homopolymers having carboxylic acid-end groups were synthesized by using mercaptoacetic acid (MAA) as the chain transfer agent. Polymerization was achieved in ethanol using azobisisobutyronitrile (AIBN) as the initiator. Average molecular weight of the homopolymer estimated by titration was 1958. This carboxylic acid-ended poly(NIPA) was then copolymerized with polyethylenimine (PEI, M(W)-2000) using a water soluble carbodiimide (EDAC). With respect to carboxyl-ended poly(NIPA), the block copolymers exhibited a pH dependent-temperature sensitivity and higher LCST values in acidic pH. Scanning tunneling microscopy (STM) images of both the homopolymer and the copolymer were obtained at 25 and 45 degrees C with tip-sample bias voltages of up to 800 mV and tunneling currents approximately 1 nA. These images showed that STM can be used to visualize both the formation of copolymer chains and their structure, and also their stimuli-responsive behavior.

Acrylamides↗

PubMed2006

Blocking the alpha 4 integrin-paxillin interaction selectively impairs mononuclear leukocyte recruitment to an inflammatory site.

Antagonists to alpha4 integrin show promise for several autoimmune and inflammatory diseases but may exhibit mechanism-based toxicities. We tested the capacity of blockade of alpha4 integrin signaling to perturb functions involved in inflammation, while limiting potential adverse effects. We generated and characterized mice bearing a Y991A mutation in alpha4 integrin [alpha4(Y991A) mice], which blocks paxillin binding and inhibits alpha4 integrin signals that support leukocyte migration. In contrast to the embryonic-lethal phenotype of alpha4 integrin-null mice, mice bearing the alpha4(Y991A) mutation were viable and fertile; however, they exhibited defective recruitment of mononuclear leukocytes into thioglycollate-induced peritonitis. Alpha4 integrins are essential for definitive hematopoiesis; however, the alpha4(Y991A) mice had intact lymphohematopoiesis and, with the exception of reduced Peyer's patches, normal architecture and cellularity of secondary lymphoid tissues. We conclude that interference with alpha4 integrin signaling can selectively impair mononuclear leukocyte recruitment to sites of inflammation while sparing vital functions of alpha4 integrins in development and hematopoiesis.

Amino Acid Substitution↗

PubMed1994

2-Mercaptoacetate and 2-deoxy-D-glucose induce Fos-like immunoreactivity in rat brain.

2-Deoxy-D-glucose (2-DG) and 2-mercaptoacetate (MA) are antimetabolic drugs that selectively antagonize glucose and fatty acid utilization, respectively, and stimulate feeding. Fos immunohistochemistry was employed to identify brain neurons activated by these drugs and to assess the role of the vagus nerve in the drug effects. Remote intravenous infusions of both MA and 2-DG induced Fos-like immunoreactivity (Fos-li) in specific brain sites, but the pattern was different for the two drugs. Mercaptoacetate induced Fos-li in the nucleus of the solitary tract (NTS), the central subnucleus of the lateral parabrachial nucleus (1PBN), the central nucleus of the amygdala (CNA, lateral part) and the dorsal motor nucleus of the vagus (DMV). Induction of Fos-li in the brain by MA was totally abolished by vagotomy. 2-Deoxy-D-glucose also induced Fos-li in the NTS, CNA (lateral part) and DMV, as well as in the external 1PBN subnucleus, locus coeruleus, paraventricular and supraoptic hypothalamic nuclei, and in scattered cells throughout the diencephalon. Induction of Fos-li by 2-DG was not blocked by vagotomy. Results suggest that 2-DG's effects on Fos-li are mediated by a direct central action, whereas MA's effects are mediated by peripheral sensory neurons. Thus, availability of glucose and fatty acids influences the activity of specific brain sites by different neural mechanisms. The correlation of Fos-immunoreactive sites with sites where lesions have been shown to cause deficits in MA- and 2-DG-induced feeding indicates that c-fos expression defines in part the central pathways involved in the metabolic control of feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

[Ecosystem of microbial flora in periodontal pockets, in vitro].

This study was designed to analyze the succession of an ecosystem of microbial flora in periodontal pockets, in vitro. Bacterial strains used in this study, were Fusobacterium nucleatum ATCC 10953, Porphyromonas gingivalis 381, Streptococcus sanguis ATCC 10557 and Streptococcus mutans OMZ 176. The bacterial cells, associated with beneficial, pathogenic or plaque forming activity, were cultured in brain heart infusion medium including hemin, vitamin-K1, L-cysteine hydrochloride and sodium thioglycollate under anaerobic condition (N2: 80%, CO2: 10%, H2: 10%). The effect of environmental Eh and pH on the growth of bacterial cells was investigated in single and mixed culture, and Eh and pH tolerance tests were also undertaken. The environmental pH decreased from pH 7.0 to pH 4.9 accompanied with the growth of S. mutans OMZ 176 and S. sanguis ATCC 10557 in both single and mixed culture. The environmental Eh increased from -308 mV to -180 mV accompanied with the growth of S. sanguis ATCC 10557. The growth of pathogenic bacteria, such as F. nucleatum ATCC 10953 and P. gingivalis 381, varied markedly with Eh and pH. Especially, the growth of P. gingivalis 381 was severely inhibited at or below pH 6.0 in an acid tolerance test, whereas the growth of F. nucleatum ATCC 10953 was strongly inhibited at Eh -100 mV in an Eh tolerance test. The oxygen generation (10.8%) was confirmed in the anaerobic culture of S. sanguis ATCC 10557. Therefore, it was suggested that hydrogen peroxide produced by S. sanguis ATCC 10557 was reduced to oxygen and water. These results suggest that the high Eh and the low pH generated from bacterial metabolism is a powerful determinant in ecology of microbial flora in periodontal pockets.

Dental Plaque↗

PubMed1983

Agglutination of murine and guinea pig peritoneal cells by alpha-L-fucose-binding lectin: Evonymus europaea.

Among lectins from Lotus tetragonolobus, Ulex europaeus I and Evonymus europaea, agglutinating cells with blood group H determinants containing L-fucose alpha 1 leads to 2-linked to subterminal D-galactose, only the last lectin agglutinates thioglycolate- and paraffin oil-stimulated murine and guinea pig peritoneal exudate cells (PEC). The agglutination is inhibited by specific inhibitors of Evonymus lectin only: lacto-N-fucopentaose I and lactose. These results suggest the presence of a determinant on the surface of PEC, containing L-fucose alpha 1-linked at the nonreducing end which is different from blood group H determinants. Nonstimulated murine peritoneal cells (PC) are not agglutinated by the lectin but become agglutinable after neuraminidase treatment. Unstimulated guinea pig PC from different animals are agglutinated to a different extent by the same lectin concentration and show increased agglutinability after neuraminidase digestion. These results show that receptor for Evonymus lectin also exists on the nonstimulated PC but access to it is hindered by sialic acid. Trypsin- and pronase-digested PEC show increased agglutinability with Evonymus lectin. These results suggest that the lectin receptor is a glycolipid. Since alpha-linked L-fucose has been suggested as a part of the macrophage receptor for migration inhibitory factor in the guinea pig (Remold, J. Exp. Med. 1973. 138: 1065), the effect of Evonymus europaea lectin on the migration of PEC was studied. It was found that lectin inhibits the migration of PEC in the capillary tube assay up to 80%.

Agglutination↗

PubMed1984

The acquisition of anti-influenza virus activity by macrophages.

Exposure of resident peritoneal macrophages or thioglycollate-induced macrophages (TG-Mø) to influenza or Sendai virus-infected spleen cell culture supernatants (MAS) resulted in macrophage activation. When normal resident macrophages were used as effector cells, both infected P815 and L929 cells were lysed in the presence of MAS. MAS-activated TG-Mø also lysed influenza virus-infected L929 cells. Histocompatibility between effector cells and target cells was not required for target cell destruction. The effector cells were plastic-adherent, phagocytic and Ia-. MAS-activated macrophages were also resistant to influenza virus infection in vitro. Both infectious and non-infectious preparations of influenza or Sendai virus preparations were effective at generating MAS. The mediator(s) which renders macrophages to become cytotoxic and resistant to infection was acid-stable, heat-labile (56 degrees C, 30 min; or 100 degrees C, 5 min), and the activity was neutralized by sheep antimouse type 1 interferon (IFN).

Animals↗

PubMed1998

Macrophage colony-stimulating factor stimulates synthesis and secretion of a mouse homolog of a human IgE-dependent histamine-releasing factor by macrophages in vitro and in vivo.

Treatment of murine resident peritoneal macrophages with macrophage-CSF (M-CSF) up-regulated the synthesis of a discrete set of proteins, including a 26-kDa protein (p26). The sequence of 20 NH2-terminal amino acids of the purified p26 was identical with the mouse homolog of a human IgE-dependent histamine-releasing factor (HRF). Among macrophage activators tested (M-CSF, granulocyte-macrophage-CSF, IL-3, TNF-alpha, IFN-gamma, and LPS), only M-CSF could up-regulate the p26 HRF synthesis by cultured macrophages. M-CSF not only increased the levels of p26 HRF mRNA and protein, but also stimulated the secretion of an N-glycosylated p26 HRF with a m.w. of 30 kDa. Repeated injections of M-CSF into mouse peritoneal cavity for 4 days elicited macrophages expressing abundant p26 HRF. A single i.p. injection of M-CSF failed to increase the p26 HRF level in peritoneal macrophages of thioglycollate-, LPS-, or adjuvant-treated mice, while M-CSF challenge to OVA-immunized mice caused macrophage infiltration and overproduction of p26 HRF, similarly as did OVA challenge. The Ag-specific priming for enhanced synthesis and secretion of p26 HRF by M-CSF was also demonstrated in cultured macrophages prepared from OVA-immunized mice. An i.p. injection of M-CSF or recombinant p26 HRF triggered eosinophil recruitment, even in the absence of the Ag, in the sensitized mice, but not in normal mice. Furthermore, recombinant p26 HRF could induce eosinophilia without marked macrophage and lymphocyte infiltrations. Our results suggest that p26 HRF secreted by M-CSF-stimulated macrophages may be an important mediator for the late phase allergic inflammation.

Animals↗