Biomedical subjects

B A Petersson

Publications and source records attributed to B A Petersson.

5 recordsLinked to original sources

PubMed1977

Enhancement by a serum factor of immunoglobulin-mediated histamine release from human leukocytes.

When serum was fractionated on Sephadex G-200, the material eluted in the second and thir major peaks had a very pronounced capacity to enhance IgE- as well as IgG-mediated histamine release from the leukocytes of both normal and allergic donors. Unseparated serum on the other hand had a low capacity to stimulate anti-IgE-induced histamine release. Besides resulting in a higher histamine release, pretreatment with serum fractions also increased the rate of histamine release. Further purification revealed that the stimulating activity of the material in the second peak was mediated by a trypsin-sensitive component, probably active in low concentration.

Animals↗

PubMed1977

Histamine release from human leucocytes. A serum factor necessary for the induction of histamine release and desensitization by protein A.

The ability of human leucocytes to release histamine on protein A treatment is lost when the cells are washed repeatedly. It is, however, possible to restore the sensitivity to protein A treatment by incubating the leucocytes in serum. Treatment of the cells with purified IgG does not restore the activity. The material responsible for the resensitization is eluted both in the second and the third protein peak when serum is chromatographed on Sephadex G-200, indicating the possible existence of several active factors. Material with low immunoglobulin content, but with retained capacity to resensitize leucocytes to release histamine on protein A treatment, was obtained by repeated chromatography of peak III material on the Sephadex G-200 column. Furthermore, material from the second and third peaks from Sephadex G-200 deprived of their IgG by passage through a protein A Sepharose or a DEAE-cellulose column had the same capacity to resensitize the leucocytes as unseparated material. When serum was separated by Pevikon block electrophoresis, most of the activity was detected in the alpha and beta regions but only little in the gamma region. The serum fractionations indicate that neither IgG nor the other immunoglobulins are the factor(s) responsible for resensitizing the leucocytes to release histamine on protein A treatment. Beside being necessary for protein A-induced histamine release, the factor (or factors) is also essential for protein A-induced desensitization of human leucocytes.

Bacterial Proteins↗

PubMed1975

Induction of histamine release and densensitization in human leukocytes.

Protein A from Staphylococcus aureus has been found to react with all human leukocyte preparations tested. In 70 percent of the experiments the reaction leads to histamine release. Furthermore, protein A treatment of cells at 37 degrees C, both in complete and Ca-2+-free medium, results in the inhibition of anti-IgE-induced histamine release in all cell preparations, indicating that protein A and anti-IgE antibodies release histamine from the same cells. This inhibition seems to be due to the blocking or exhaustion of a step in the biochemical pathway, leading to histamine release activated by both protein A and anti-IgE. In some cell preparations desensitization but no histamine liberation is induced by protein A. No inhibition occurs if the protein A treatment is performed at 4 degrees C. It is concluded that protein A elicits histamine liberation and desensitization by acting on IgG present on the surface of the basophil granulocytes. Treatment of leukocytes at 37 degrees C with anti-IgE antibodies, or F(ab)2 fragments from such antibodies, also results in an inhibition of a subsequent anti-IgE-induced histamine release. Desensitization with low doses of anti-IgE results in an inhibition of the same type as that obtained with protein A. Supraoptimum amounts of anti-IgE or high amounts of monovalent Fab fragments from anti-IgE immunoglobulin G give an inhibition that could be due to a competition between the sensitizing and the challenging agents for combining with cell fixed IgE molecules. This inhibition is independent of temperature and calcium concentration.

Animals↗

PubMed1975

Induction of histamine release and desensitization in human leukocytes.

Histamine release from normal human leukocytes can be induced by anti-IgE or protein A from Staphylococcus aureus. After incubation in buffer at 37 degrees C for various time intervals or repeated washings with buffer, or both procedures, the leukocytes lose most of their reactivity to protein A, whereas the reactivity to anti-IgE is unaltered. Cells deprived of their protein A reactivity can be induced to release histamine by IgG complexed with protein A. Maximal release (23%-81%) from 0.6-1.0 times 10(7) leukocytes per ml is obtained if the mixture contains 1-2 mug protein A and 8-16 mug IgG per ml. The ratio between protein A and IgG in the most active mixtures is 1:8 or 1:16 on a weight basis, which corresponds to 2-4 IgG molecules per protein A molecule. Heat treatment does not destroy the capacity of IgG to mediate histamine release. Mixtures of protein A and the Fc part of IgG can also initiate the release. Futhermore, it is shown that the protein A-IgG mixture and anti-IgE induce cross-desensitization to each other. This indicates that, like cell-bound IgG, IgG in complex with protein A triggers partially the same reaction sequence as IgE.

Antibodies, Anti-Idiotypic↗

PubMed1975

Induction of histamine release and desensitization in human leukocytes. Effect of anaphylatoxin.

Hog anaphylatoxin (AT) in concentrations from 0.5 to 5 mug/ml gives a dose-dependent histamine release from human leukocytes. Concentration of 100 mug/ml AT give the same high histamine release as 5 mug/ml. This is in contrast to the histamine release obtained with anti-IgE or allergen, which give low histamine release with high doses. The histamine release obtained with AT is completed in 20 sec and the reaction is temperature- and calcium-dependent. Treatment of cells with AT in the presence or absence of calcium makes them insensitive to another challenge with AT. Such treated cells are fully responsive, however, to challenge with anti-IgE if the pretreatment has been performed in the absence of calcium. This, together with the calcium- and temperature-dependence indicates that the AT-induced histamine release is nontoxic. Treatment of cells with AT in the presence of calcium induces, besides histamine release, decrease in sensitivity to anti-IgE, indicating that both AT and anti-IgE release histamine from the same cells. We discuss to what extent AT and cell-bound Ig share intracellular mechanisms for induction of histamine release.

Anaphylaxis↗