Reagin-like Antibodies in Animals Immune to Helminth Parasites

Ogilvie, Bridget M.

doi:10.1038/204091a0

Cited by 141 publications

(58 citation statements)

References 8 publications

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“…Four to six weeks later the animals were killed. At this time there is a high titre of reaginic antibodies in the serum of the infected rats and the target cells of the lung tissue are sensitized with cell bound antibody (Ogilvie, 1964 (Mota, 1964;Sheard & Blair, 1970). Eight to 12 days later the rats were killed, their lungs perfused by the method described for guinea-pig lungs (Piper & Vane, 1969a) and challenged by injection of 2 mg of ovalbumen into the pulmonary artery.…”

Section: Methodsmentioning

confidence: 99%

The release of spasmogenic substances from human chopped lung tissue and its inhibition

Piper¹,

Walker²

1973

British J Pharmacology

107

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Summary Human lung tissue, passively sensitized with reaginic antibodies, released prostaglandins E1, E2 and F2α in addition to histamine and slow reacting substance (SRS‐A), when exposed to the appropriate antigen. No rabbit aorta contracting substance (RCS) was detected. Experiments with rats and guinea‐pigs showed that the release of RCS is not confined to anaphylactic reactions mediated by non‐reaginic antibodies but may be a feature of anaphylaxis in guinea‐pigs alone. Human lung tissue gently agitated with a blunt nylon rod liberated an E‐type prostaglandin and RCS in addition to histamine and SRS‐A. Human isolated bronchial muscle was contracted by RCS. Disodium cromoglycate antagonized the release of prostaglandins during anaphylaxis but not during agitation of human lung tissue, whereas indomethacin blocked the release of prostaglandins during agitation and anaphylaxis. The release of an E‐type prostaglandin during anaphylaxis in human lung tissue, which inhibits the further release of histamine could be another example of the regulatory role of prostaglandins in body functions.

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Section: Methodsmentioning

confidence: 99%

The release of spasmogenic substances from human chopped lung tissue and its inhibition

Piper¹,

Walker²

1973

British J Pharmacology

107

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“…Sprague-Dawley rats were infected by a subcutaneous injection of 3000 larvae of N. brasiliensis (19). The rats were reinfected with 4000 larvae 4-5 weeks after the primary infection.…”

Section: Methodsmentioning

confidence: 99%

Induction of calcium flux across the rat mast cell membrane by bridging IgE receptors.

Ishizaka¹,

Foreman²,

Sterk³

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

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Rabbit antibody against IgE receptors or its F(ab')% fragments induced an increase of 45Ca uptake into normal mast cells, and this process was accompanied by histamine release. (14,15) have shown that stimulation of rat mast cells with an antigen-antibody reaction, dextran, or concanavalin A induces an increase in the uptake of 45Ca, which is accompanied by histamine release. In view of these findings, the present experiments were undertaken to determine whether the bridging of IgE receptors on mast cells by divalent antireceptor antibodies may induce 45Ca uptake. MATERIALS AND METHODSAntireceptor Antibodies and Antiimmunoglobulins. Antireceptor antibody used in the present experiments was the same material as that described in a previous article (10). Briefly, rat basophilic leukemia (RBL) cells were saturated with monoclonal rat IgE and then solubilized in Nonidet P-40. Solubilized IgE-receptor complexes were precipitated by rabbit anti-IgE antibodies, and a rabbit was immunized with the precipitates included in complete Freund's adjuvant. Antibodies against cell-surface components were purified by using RBL cells as an immunosorbent, and these partially purified antibodies were rendered specific for mast cells by absorption with mast-cell-depleted peritoneal exudate cells. Analysis of membrane components that bound to the antibody preparation (anti-RBL) by sodium dodecyl sulfate gel electrophoresis showed that the major antibodies in anti-RBL were antireceptor antibodies (11). Further analysis indicated that the antibodies were directed toward the binding site for IgE in the receptor molecules (11). The F(ab')2 fragments of anti-RBL were obtained by pepsin digestion, and these fragments were split into Fab' monomer by reduction and alkylation (12). Because the protein concentration of purified anti-RBL was low (1.6 mg/ml), 8-fold excess of normal rabbit IgG was added to the antibody preparation before digestion.The IgG fraction of a goat or a rabbit antiserum monospecific for rat IgE (anti-IgE) and purified goat antibodies specific for rabbit IgG were the same preparations as those described in a previous article (10).Purification of Mast Cells. Mast cells were obtained from peritoneal cells of Sprague-Dawley rats (Holtzman Co., Madison, WI) by the method of Bach et al. (16) with slight modifications (17). Purity of mast cell preparations was 90 + 3%, and the viability of the cells, as assessed by trypan blue exclusion test, was higher than 97%.Measurement of 45Ca Uptake. The method described by Foreman et al. (15) was followed. Purified mast cells were suspended in Tyrode's solution (pH 7.0) containing 1 mM CaC12, 0.5 mM MgCI2, 5 mM Hepes, 5 mM 2-(N-morpholino)ethanesulfonic acid (Mes) (Sigma), and 0.5 g of gelatin per liter. Unless otherwise specified, phosphatidylserine (50 ,ug/ml) (Supelco, Bellefonte, PA) was dispersed in the solution by sonication. Measurement of 45Ca uptake was set up in duplicate. One hundred microliters of Versilube F50 silicone oil (General Electric, Waterford, NY) was p...

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“…IgE antibodies io P. falciparum A common cause of IgE elevation in third world countries is helminthic infection [29][30][31]. In order to substantiate a possible involvement of malaria in IgE induction, sera from the Liberian donors included in Table 1 were analysed in ELISA for antihodies binding to F. falciparum antigens.…”

Section: Levels Of Total Igementioning

confidence: 99%

IgE elevation and IgE anti-malarial antibodies in Plasmodium falciparum malaria; association of high IgE levels with cerebral malaria

Perlmann

Helmby

Hagstedt

et al. 1994

Clinical and Experimental Immunology

113

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SUMMARYIn the course of studying immunoregulation in human Plasmodium falciparum malaria we have investigated IgE levels and IgE anti-plasmodial antibodies in children and adults from areas of high malaria endeniicity in both Africa and Asia. On average, 85% of all donors had significantly elevated levels of total IgE. A fraction of the IgE had anti-plasmodial activity as revealed by ELISA with lysates of infected crythrocytes as antigen. Using synthetic peptides representing antigenic regions of two major plasmodial blood stage antigens, IgE antibody concentrations ranged from 5 to 15 ng/ml serum for each of the peptides. On average, the concentrations of the corresponding IgG antibodies were x500-I000 higher. Immunobiotting of parasite lysates showed that most donors had IgE antibodies against one or several of a restricted number of plasmodial polypeptides, with antibodies against an antigen of moi.wt 45 kD already being present in all donors at an early age. Donors having IgE antibodies to particular antigens also frequently had corresponding IgG4 arffWvdies. reflecting underlying IL-4-dependent cellular mechanisms controlling formation of these isotypes. As infection with other parasites sueh as helminths is known lo induce IgE elevation, the results do not prove that plasmodial infections were the primary cause of IgE induction. However, the importance of plasmodial infection for IgE elevation was supported by the finding of significantly higher levels of IgE., but not of IgG, in children with cerebral malaria compared with patients with uneomplicated disease.

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Reagin-like Antibodies in Animals Immune to Helminth Parasites

Cited by 141 publications

References 8 publications

The release of spasmogenic substances from human chopped lung tissue and its inhibition

The release of spasmogenic substances from human chopped lung tissue and its inhibition

Induction of calcium flux across the rat mast cell membrane by bridging IgE receptors.

IgE elevation and IgE anti-malarial antibodies in Plasmodium falciparum malaria; association of high IgE levels with cerebral malaria

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