Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.17 (
lysozyme
)
21,489
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
1. The de novo synthesis of arginase was much higher in murine than in rat peritoneal macrophages. This process was inhibited irreversibly by protein synthesis inhibitors and reversibly by glycolysis blockers. 2. Rat macrophages produce more
nitric oxide
(NO) than murine cells. NO production was inhibited by the inhibitors of protein synthesis or glycolysis. 3. The loading of macrophages by exogenous arginine for 24 hr in vitro resulted in the increase of arginase and nitrite in macrophages to different extents. 4. No great differences in
lysozyme
production was observed. 5. The proportion of arginine taken up and incorporated is contrasted in murine and rat macrophages.
...
PMID:Inverse relation in the de novo arginase synthesis and nitric oxide production in murine and rat peritoneal macrophages in long-term cultures in vitro. 147 64
We tested the effect of
lysozyme
on the nasal mucosa in a controlled double-blind in vivo study. The administration of non-pathogenic vaccine strains of living measles virus and of living Vivotif bacteria (attenuated Salmonella typhi) to 14 healthy subjects showed that
lysozyme
possesses a clear antimicrobial and antiviral effect.
HNO
1989 May
PMID:[The antimicrobial effect of lysozyme on nasal mucosa]. 265 60
72 patients suffering from recurrent tonsillitis, and ten with infectious mononucleosis were compared by morphological and immunological studies. The distribution of Ig-containing plasma cells (IgA, IgG, IgM), lambda- and kappa-chains,
lysozyme
and Alpha-1-antitrypsin in tonsils was determined by the unlabelled antibody peroxidase-antiperoxidase method and correlated with the structure of the tonsils (follicles, interfollicular area, and reticular epithelium). While recurrent tonsillitis was associated with slight follicular hyperplasia, infectious mononucleosis was characterised by a marked distortion of the tonsillar architecture, reduction in the number of follicles and a mixed cellular proliferation. The cellular infiltration was composed of small, well differentiated lymphocytes, atypical lymphocytes (Downey cells), plasma cells, immunoblasts, and a variable number of pleomorphic immunoblasts (Reed-Sternberg-like-cells). The binucleated or multinucleated immunoblasts contained IgA, IgG, and IgM. Ig-producing cells occurred in all compartments. In recurrent tonsillitis most were found in the reticular epithelium, but in infectious mononucleosis their density was highest in the interfollicular area. There was a general prominence of IgG cells, confirming that the tonsils resemble lymph nodes more closely than the lymphoid tissue of the alimentary tract. Cells containing lambda and kappa chains were found in all follicle centres and extra-follicular areas. They gave evidence of polyclonality in both diseases. Lysozyme and Alpha-1-antitrypsin were present only in the vessels.
HNO
1985 Feb
PMID:[Comparative immunocytochemical studies of recurrent tonsillitis and infectious mononucleosis]. 388 56
Mouse hen egg-white
lysozyme
-specific anaphylaxis was estimated by monitoring changes in blood pressure by using a tail-cuff method. Stimulation of histamine H1 receptors of the vascular endothelium was suggested to be critical for mouse anaphylactic hypotension, because pretreatment with diphenhydramine but not with cimetidine completely inhibited the hypotension.
Nitric oxide
(NO) was indicated to play an important role in mouse anaphylaxis, because NG-nitro-L-arginine methyl ester, a NO synthase inhibitor, significantly blocked the hypotension while a large amount of L-arginine, a precursor of NO synthesis, restored the hypotension.
...
PMID:Participation of nitric oxide in mouse anaphylactic hypotension. 816 57
Macrophage inflammatory and immune functions were characterised in red deer (cervus elaphus), for use as a model for natural infection with bovine tuberculosis. Highly enriched populations of deer macrophages were obtained from 14 day cultures of plastic-adherent peripheral blood mononuclear cells. Cervine macrophages produced superoxide anion in response to respiratory burst stimuli (serum-opsonised zymosan and phorbol myristic acetate), but
nitric oxide
production could not be detected under the conditions tested. The lysosomal enzymes acid phosphatase and
lysozyme
were detected at the intercellular and extracellular level. Stimulation with bacterial lipopolysaccharide extract (Escherichia coli LPS) enhanced the production of superoxide and acid phosphatase with a peak increase in activity observed after 2h. Production of interleukin 1 (IL-1) and tumour necrosis factor (TNF), determined using cytokine-sensitive cell lines and mRNA analysis (Northern blotting), indicated maximal secretion of both cytokines after 24 h stimulation with LPS, preceded by a peak in message accumulation at 2-6 h post-stimulation. Cervine macrophages stimulated proliferative responses in T cell-enriched lymphocyte populations derived from the peripheral blood of autologous animals that had been primed to mycobacterial antigens (Mycobacterium bovis Bacille Calmette-Guerin, BCG). Macrophages were able to stimulate responses after pulsing with particulate (BCG) or soluble (purified protein derivative) mycobacterial antigens. These results indicate that macrophage inflammatory and immune responses in red deer are similar to those in other mammalian species, and that macrophages may play an important role in resistance to mycobacterial infection.
...
PMID:Macrophage function in deer. 867 37
It has been found that certain antineoplastic drugs impart their function with a distinct duality. Besides being tumoricidal, they are capable of acting as immunopotentiator. This led us to investigate the effect of cytosine arabinoside (CA), vincristine sulphate (VS), cyclophosphamide (CS), mitomycin C (MMC), hydroxy urea (HU) and lipopolysaccharide (LPS) on a macrophage cell line P388D1. Supernatants collected from P388D1 cells treated with CA, VS, CS, MMC, HU or LPS demonstrated enhanced production of tumor necrosis factor (TNF) confirmed by bioassay on L929 tumor target cells and increased interleukin-1 (IL-1) production by standard thymocyte proliferation bioassay. Also, supernatants showed increased amounts of
nitric oxide
and
lysozyme
using Griess reaction and reduction in turbidity of Micrococcus lysodeikticus, respectively. The above findings demonstrate that these drugs may be used not only as chemotherapeutic agents but also as macrophage-activating agents.
...
PMID:Activation of P388D1 macrophage cell line by chemotherapeutic drugs. 909 41
Tyrosine nitration is a covalent posttranslational protein modification derived from the reaction of proteins with nitrating agents. Protein nitration appears to be a selective process since not all tyrosine residues in proteins or all proteins are nitrated in vivo. To investigate factors that may determine the biological selectivity of protein tyrosine nitration, we developed an in vitro model consisting of three proteins with similar size but different three-dimensional structure and tyrosine content. Exposure of ribonuclease A to putative in vivo nitrating agents revealed preferential nitration of tyrosine residue Y(115). Tyrosine residue Y(23) and to a lesser extent residue Y(20) were preferentially nitrated in
lysozyme
, whereas tyrosine Y(102) was the only residue modified by nitration in phospholipase A(2). Tyrosine Y(115) was the residue modified by nitration after exposure of ribonuclease A to different nitrating agents: chemically synthesized peroxynitrite,
nitric oxide
, and superoxide generated by SIN-1 or myeloperoxidase (MPO)/H(2)O(2) plus nitrite (NO(-2)) in the presence of bicarbonate/CO(2). The nature of the nitrating agent determined in part the protein that would be predominantly modified by nitration in a mixture of all three proteins. Ribonuclease A was preferentially nitrated upon exposure to MPO/H(2)O(2)/NO(-2), whereas phospholipase A(2) was the primary target for nitration upon exposure to peroxynitrite. The data also suggest that the exposure of the aromatic ring to the surface of the protein, the location of the tyrosine on a loop structure, and its association with a neighboring negative charge are some of the factors determining the selectivity of tyrosine nitration in proteins.
...
PMID:Factors determining the selectivity of protein tyrosine nitration. 1054 3
In order to explore the depressant action of ambroxol, a bronchial expectorant, on the activated alveolar macrophage responses, its effect on lipopolysaccharide (LPS)- or N-formyl-methionyl-leucyl-phenylalanine (fMLP)- stimulated free radical production and granule enzyme release by rat lung alveolar macrophages was investigated. Ambroxol attenuated the 100 ng/ml LPS- or 1 microM fMLP-stimulated superoxide, H(2)O(2)and
nitric oxide
production and releases of acid phosphatase and
lysozyme
by alveolar macrophages. Ambroxol attenuated phorbol myristate acetate-stimulated superoxide and
nitric oxide
production that was inhibited by 100 nM staurosporine. N,N-dimethylsphingosine (DMS, 4.5 and 9 microM) alone stimulated superoxide production by macrophages, while 45 microM of the compound did not show a stimulatory effect. However, DMS decreased
nitric oxide
production in a dose-dependent manner. Ambroxol did not alter the DMS effect on free radical production that was affected by 10 microM genistein. A preincubation of macrophages with ambroxol (10 and 100 microM), staurosporine and genistein attenuated the elevation of [Ca(2+)](i)caused by LPS. The results suggest that ambroxol exerts a depressant effect on LPS- or fMLP-stimulated free radical production and granule enzyme release by rat alveolar macrophages, which may be attributed to its inhibitory action on the activation process, protein kinase C, but its action on protein tyrosine kinase is not suggested.
...
PMID:Depressant effects of ambroxol on lipopolysaccharide- or fMLP-stimulated free radical production and granule enzyme release by alveolar macrophages. 1054 83
Newcastle Disease Virus (NDV), an agent with interesting immune stimulatory and anti-tumor activity, was investigated for its capacity to activate anti-tumor activity in murine macrophages in vitro and in vivo. Direct macrophage activation was seen under a variety of experimental conditions using two different strains of NDV, different sources of macrophages (spleen and peritoneum) and different strains of mice (DBA/2, C57BL/6, 615). Various macrophage enzymes (ADA, iNOS,
lysozyme
, acid phosphatase) became upregulated and anti-tumor effector molecules such as
nitric oxide
(NO) and TNF-alpha were found in the supernatant. NDV activated macrophages performed anti-tumor activity in vitro such as anti-tumor cytostasis and anti-tumor cytotoxicity. The cytotoxic anti-tumor activity was broad and active against all tumor lines tested including mammary carcinoma, lung carcinoma, mastocytoma and immune escape variants (lymphoma). Macrophage activation via BCG/LPS also caused a broad range anti-tumor cytotoxic activity while activation via mixed lymphocyte culture conditioned medium had restricted anti-tumor activity. Anti-tumor activity of NDV activated macrophages could be transfered in vivo. Transfer of macrophages which had not been appropriately activated exerted either no effect or a tumor growth augmenting effect. Repeated intravenous transfer of NDV activated macrophages exerted a significant suppressive effect on pulmonary metastases in a mammary carcinoma tumor model as well as in a lung carcinoma model. Taken together these results demonstrate that NDV can strongly activate macrophages to perform anti-tumor activities in vitro and in vivo.
...
PMID:Newcastle disease virus activates macrophages for anti-tumor activity. 1063 82
The process of degranulation of mast cells and neutrophils contributes to inflammatory disorders. Activation of microglial cells and macrophages is believed to be involved in inflammatory, infectious and degenerative diseases of the CNS. Combining the potent inhibition of chemical mediators released by the degranulation of mast cells or neutrophils and from the activated microglial cells or macrophages, would lead to a promising anti-inflammatory agent for the treatment of peripheral and central inflammation. A series of chalcone derivatives have been reported to have potent anti-inflammatory activity. In an effort to continually develop potent anti-inflammatory agents, novel series of chalcones, 2'-hydroxy- and 2',5'-dihydroxychalcones were synthesized and their inhibitory effects on the activation of mast cells, neutrophils, microglial cells and macrophages were evaluated in-vitro. The chalcones were prepared by Claisen-Schmidt condensation of appropriate acetophenones with an appropriate aromatic aldehyde. The alkoxychalcones were prepared with appropriate hydroxychalcones and alkyl iodide and the dihydroxychalcones were prepared by hydrogenation of an appropriate chalcone with Pd/C. Almost all of the hydroxychalcones exhibited potent inhibitory effects on the release of beta-glucuronidase and
lysozyme
from rat neutrophils stimulated with formyl-Met-Leu-Phe/cytochalasin B (fMLP/CB). Of the hydroxychalcones, compound 1 was the most potent inhibitor of the release of beta-glucuronidase (IC50=1.6+/-0.2 microM) and
lysozyme
(IC50=1.4+/-0.2 microM) from rat neutrophils stimulated with fMLP/CB. Almost all of the 2',5'-dialkoxychalcones exhibited potent inhibitory effects on
nitric oxide
(NO) formation from murine microglial cell lines N9 stimulated with lipopolysaccharide (LPS). Of these, compound 11 showed the greatest effect (IC50=0.7+/-0.06 microM). The present results demonstrated that most of the chalcone derivatives have an anti-inflammatory effect. The inhibitory effects of dialkoxychalcones, 10-12 on inflammation are probably not due to the inhibition of mast cells and neutrophil degranulation, but are mediated through the suppression of NO formation from N9 cells.
...
PMID:Synthesis and anti-inflammatory effect of chalcones. 1071 46
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