Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibody responses were measured in a volunteer infected four times with Necator americanus over a 27-month period. The main source of antigen was culture fluid in which living adult N. americanus had been maintained for several days. Antibodies to worm acetylcholinesterase and IgE antibodies were detected only with this material, but antibodies were identified by the enzyme-linked immunosorbent (ELISA) assay, with either adult worm secretions or extracts of third-stage infective larvae. The total serum IgE level fell after the first infection, but although it then increased during subsequent infections, it never rose above 600 U per ml. None of the antibody responses suppressed the rat of worm development to maturity, or reduced the fecundity of the parasites. However, it is suggested that the development of the immune response may be associated with the waning of the severe gastro-intestinal symptoms which were experienced in this infection, and which are frequently characteristic of hookworm infections.
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PMID:Antibody responses in self-infections with Necator americanus. 63 80

Histamine release from the basophil leucocytes of patients with apparently non-immune, anaphylactiod reactions to neuromuscular blockers ( NMB ) has been studied in vitro. Substantial release was obtained in the majority of patients with clinical reactions, with little or no release in normal subjects. The chemical specificity and selectivity varied in individual patients: each individual reacting to one agent or a particular combination of NMB drugs. The test was of considerable diagnostic and predictive value. We studied some of the characteristics of the histamine release process and the effect of certain modulators. The findings strongly suggest a non-cytotoxic secretory process requiring the presence of two quaternary ammonium groups as suggested by the rarity of release with tubocurarine; inhibition of succinyldicholine (suxamethonium)-induced histamine release by serum cholinesterase treatment, acetylcholine and tubocurarine; and the bell-shaped dose-response curve, particularly with suxamethonium. Histamine release by all NMB was completely inhibited in calcium-free medium, and markedly potentiated by deuterium oxide, a microtubule stabilizer. Both tachyphylaxis (by prior exposure to the specific agent in absence of calcium), and cross-tachyphylaxis with anti-IgE were elicited.
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PMID:Characteristics of basophil histamine release by neuromuscular blocking drugs in patients with anaphylactoid reactions. 620 65

Liver biopsies of a 58-year-old clinically healthy patient with a hepatomegaly and intracisternal PAS-negative globular hyaline bodies were immunofluorescent-optically examined for the content of the complement components C 1 q, C 4, C 9, C 1-inactivator, C 3-activator. Further examinations were performed for fibrinogen, IgG, IgA, IgM, IgD, IgE, L-chain (type chi and lambda), alpha 1-antitrypsin, alpha 1-fetoprotein, alpha 1- and alpha 2-glycoprotein, cholinesterase, ceruloplasmin, myoglobin, hemopexin, HBsAg and HBsAg. Th inclusion bodies reacted with antisera against the complement components C 4, C 3 and C 3-activator, as also identified by double immunofluorescence. Probably this is a disturbance of the protein metabolism of the liver cell with abnormal complement storage in the presence of normal total complement and normal complement components in the serum.
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PMID:Storage of the complement components C4, C3, and C 3-activator in the human liver as PAS-negative globular hyaline bodies. 628 41

Various parasitic nematodes secrete acetylcholinesterase (AChE). In this study, the localization of AChE in the nematode Nippostrongylus brasiliensis and the secretory forms of AChE in culture fluid were examined. A thiocholine method revealed that AChE activity was localized in the subventral glands, which have a secretory and excretory function via a duct connected to the excretory pore. By electron microscopy, AChE activity was found mainly in the matrix of secretory granules, and sometimes in the Golgi apparatus in the subventral gland cells. These results show that nematode AChE is produced and stored in the subventral glands. Monoclonal antibodies against AChE of human erythrocytes or electric rays also bound to the nematode subventral gland, suggesting immuno-cross-reactivity of AChE among these species. When AChE activity in the nematode excretory-secretory product was examined by SDS polyacrylamide gel electrophoresis combined with the thiocholine method, intense activity was demonstrated as a single band at 74 kDa. Immunoblot analysis showed specific recognition of this molecule by IgE and IgG1 antibodies, but not by IgG2a antibody, in nematode-infected rat sera. These results indicate that the nematode AChE molecule produced in and secreted from the subventral glands is antigenic for the production of IgE/IgG1 in host animals.
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PMID:Immunocytochemical localization of secretory acetylcholinesterase of the parasitic nematode Nippostrongylus brasiliensis. 775 Jan 37

Chronic obstructive pulmonary disease (COPD) is a disease involving either or both of chronic bronchitis and emphysema. In the elderly, bronchial asthma is usually called chronic asthma because of sustained asthma attacks and resistance to therapy. Although the absolute value of IgE is low in the asthma in the elderly, IgE values correlated to the symptoms of asthma in the elderly. Therefore, asthma in the elderly is supposed to be primarily caused by allergic reactions. Airway epithelium products histamine methyl-transferase (HMT) and cholinesterase. Allergic reactions and/or virus infection in the airway epithelium reduce productions of these enzymes, which exacerbate bronchoconstriction. Steroid hormones increase these enzymes and relieve bronchoconstriction. Silent aspiration may exacerbate asthma attack in the night and recurrent cough and sputum in COPD. Macrolide antibiotics relieve chronic infections in the elderly. Plural constriction against bullae using thoracoscopy reduce dyspnea dramatically in emphysema.
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PMID:[Clinical strategy of chronic obstructive pulmonary disease in the elderly]. 811 44

We have produced two lines of transgenic mice in which the expression of temperature-sensitive SV-40 large T antigen is targeted to bone marrow megakaryocytes via the platelet factor 4 (PF4) tissue-specific promoter. The progeny of these transgenic mice were observed for about 3 mo, and no malignancies were detected over this period of time. The offspring of these transgenic mice, 6- to 12-wk of age, served as a source of bone marrow cells, which upon in vitro cultivation at the permissive temperature yielded immortalized cell lines (MegT). At the permissive temperature, MegT cells exhibit the characteristics of early 2N and 4N megakaryocytes which include the presence of specific gene products such as PF4, glycoprotein IIb, acetylcholinesterase, and CD45 as well as the absence of molecular markers of other cell lineages such as the macrophage marker Mac-1, the T helper cell marker CD4, the mast cell marker IgE, the T cell marker CD2 or the erythroid cell marker alpha-globin. The inactivation of the oncogene by a shift of temperature from 34 degrees to 39.5 degrees C produces a reduction in the frequency of the 2N cells, in conjunction with the appearance of 8N and 16N cells, consisting of 27 and 3% of total cells, respectively. Thus, we have generated hematopoietic cell lines that are trapped in the early stages of megakaryocyte commitment, but able to undergo part of the normal program of terminal differentiation.
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PMID:Targeted expression of a conditional oncogene in hematopoietic cells of transgenic mice. 825 49

Human bronchi were incubated in organ baths to measure histamine release. The calcium ionophore A23187 (10 mumol/L; 1 min) stimulated histamine release by 148 +/- 28% (n = 11) above the prestimulation level but was ineffective in epithelium-denuded bronchi. Neither bradykinin (0.1 mumol/L) nor compound 48/80 (10 micrograms/ml) triggered the release of histamine from epithelium-intact bronchi. Acetylcholine did not affect spontaneous histamine release (about 2 nmol/g x 5 min) but inhibited A23187-evoked histamine release in an atropine-sensitive manner. Already a concentration as low as 0.1 nmol/L acetylcholine was effective, the maximal inhibition (by 89%) occurred at 100 nmol/L, whereas a concentration of 10 mumol/L acetylcholine was ineffective. Oxotremorine (1 nmol/L), a stable agonist at muscarinic receptors, suppressed stimulated histamine release completely. Physostigmine (0.1 mumol/L), an acetylcholinesterase inhibitor, reduced A23187-evoked histamine release by 58%. Antihuman IgE antibody stimulated histamine release by 127 +/- 30% (n = 6) above the prestimulation level. Acetylcholine (100 nmol/L) inhibited also the immunologically evoked histamine release by 70%. In conclusion, the present experiments provide a model to characterize mast cells that are localized in or close to the airway surface epithelium. Acetylcholine via muscarinic receptors strongly inhibits the releasability of these mucosal mast cells being among the first cells to interact with inhaled antigens and environmental agents. The inhibitory action of physostigmine indicates the involvement of endogenous, probably non-neuronal acetylcholine expressed in airway epithelial cells.
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PMID:Acetylcholine via muscarinic receptors inhibits histamine release from human isolated bronchi. 927 14

An animal model of food allergy represents an important tool for studying the mechanisms of induction and repression of an allergic reaction, as well as for the development of an immunotherapy to prevent or minimize such an adverse reaction. IgE and IgG1 (Th2 response) vs. IgG2a (Th1 response) are good markers for the induction of an allergic response in mice. Nevertheless, while the total serum concentrations of these isotypes are easy to measure using classical sandwich immunoassays, this is not the case for allergen-specific isotypes. To develop an animal model of allergy to bovine beta-lactoglobulin (BLG), we set up quantitative assays for total and for allergen-specific IgE, IgG1 and IgG2a. Microtiter plates coated either with anti-isotype antibodies (Abs) or with allergen were used for Ab capture, while anti-isotype Fab' fragments coupled to acetylcholinesterase were used for visualization. These assays of anti-BLG specific Abs are original in two ways. First, assay calibration is performed using anti-BLG specific mAbs, thus allowing good quantification of the different isotypes and subclasses of serum antibodies. Second, the detection of all anti-BLG specific Abs, i.e., those recognizing both the native and denatured forms of the protein, is achieved through indirect coating of BLG using biotin-streptavidin binding. The present assays are quantitative, specific to the isotype (cross-reactivity <0.5%), very sensitive (detection limit in the 10 pg/ml range), and reproducible (coefficient of variation less than 10%). Applied to the humoral response in mice sensitized with BLG adsorbed on alum, these assays proved to be a very useful tool for monitoring high IgE-responder mice following BLG immunization, and for an immunotherapy directed at polarizing the immune response.
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PMID:Evaluation of a high IgE-responder mouse model of allergy to bovine beta-lactoglobulin (BLG): development of sandwich immunoassays for total and allergen-specific IgE, IgG1 and IgG2a in BLG-sensitized mice. 1067 54

Organophosphorous pesticides exert sensitizing effects. Our investigations in workers of the chlorfenvinphos production department showed frequent incidence of the upper respiratory tract allergy as well as diminished specific airways conductance. The aim of the study is to assess serum immunoglobulin E concentration in the workers of the chemical plant department producing chlorfenvinphos. The study covered the entire staff of the department:--35 men aged 25-55 years, employed for 1-15 years. Chronic bronchitis was diagnosed in 13 (37.1%) workers; in none of the subjects examined bronchial asthma was found. Spirometry showed a lower Tiffeneau's index in 5 (14.3%) and impaired specific airways conductance in 11 (31.4%) workers. Air chlorfenvinphos concentration in the work environment did not exceed MAC level, the average concentration was 0.0008-0.0018 mg/m3, and the erythrocyte acetylcholinesterase activity was within normal range. Serum IgE concentration was evaluated with the enzyme immunoassay (Enzymun-Test IgE from Boehringer, Cat. No. 1289071), the results were compared with those of a control group of 30 healthy male inhabitants of the region, professionally not exposed to chemical noxes. Mean serum IgE concentration in the workers (109.6 +/- 120.0 IU/ml) was significantly (p < 0.01) higher as compared to the control group (51.1 +/- 36.4 IU/ml). In 14 (40.0%) workers the IgE concentration exceeded 100 IU/ml, whereas in the control group only in 4 (13.3%) people the IgE level was elevated. The results of our investigations provide support for an essential role of type I hypersensitivity reaction in the pathogenesis of inflammatory changes in the respiratory system caused by chlorfenvinphos.
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PMID:[Serum immunoglobulin E concentration in workers producing chlorfenvinphos]. 1195 84

This review describes the effects of realization of the central and peripheral "cholinergic antiinflammatory pathway" in a model of endotoxic and anaphylactic shock. Under endotoxic shock conditions, a pharmacological correction by means of the central m-cholinomimetic action (electrical stimulation of the distal ends of nervus vagus after bilateral cervical vagotomy, surgical implantation of the stimulant devise, activation of efferent vagal neurons by means of muscarinic agonist) is directed toward the elimination of LPS-induced hypotension. During the anaphylaxis, peripheral effects of the cholinergic system induced by blocking m-AChR on the target cells (neuronal and non-neuronal lung cells) and acetylcholinesterase inhibition are related to suppression of the bronchoconstrictor response. The role of immune system in the pathogenesis of endotoxic shock is associated with the production of proinflammatory cytokines by macrophages, increase in IgM concentration, and complement activation, while the role in the pathogenesis of anaphylactic shock is associated with IgE, IgG1 augmentation. Effects of B cell stimulation may be important in hypoxia and in the prophylaxis of stress ulcers and other diseases. Plasma proteins can influence the effects of the muscarinic antagonist methacine: IgG enhance its action while albumin and CRP abolish it.
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PMID:[Modulation of the cholinergic system during inflammation]. 1848 13


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