Antigen Induced Release of Histamine and SRS-A from Human Lung passively sensitized with Reaginic Serum

Sheard, Philip W.; Killingback, P. G.; Blair, Allison

doi:10.1038/216283a0

Cited by 114 publications

(26 citation statements)

References 6 publications

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“…Appropriate tests with isolated cells or cell cultures there fore provide a remarkable advantage. The procedure whereby antigen-induced hista mine is released from passively sensitized hu man lung ensures the differentiated assess ment of the efficacy and mode of action of those drugs which are being used in the treatment of bronchial asthma [19,21,23,26]. This is supported by the results of the following experiments using fenoterol, one of the 'second generation' adrenaline deri-vates which exhibit predominantly selective /?2-receptor stimulation.…”

supporting

confidence: 66%

Immunological Release of Histamine from Human Lung

Morr¹

1979

Respiration

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Human lung tissue passively sensitized with anti-grass pollen IgE antibodies release histamine upon exposure to specific grass pollen antigen. Fenoterol, a β₂-sympathomimetic stimulator drug, is shown to be a potent inhibitor of antigen-induced release of histamine. This inhibitory effect occurred with fenoterol concentrations of 2 × 10^-8 to 1 × 10^-7M, and was determined by 67 and 95%, respectively. Thus, the β₂-receptor stimulator fenoterol is a valuable drug for treating allergic bronchial asthma since it exhibits a combination of prophylactic and direct therapeutic properties.

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confidence: 66%

Immunological Release of Histamine from Human Lung

Morr¹

1979

Respiration

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“…Studies of respiratory allergic disease using chopped lung fragments have provided substantial insight into the mechanisms of mediator release by antigenic stimuli (1). This system was modified by Lewis et al (2) who introduced techniques to disperse the tissue into single cell suspensions using the proteases elastase, collagenase, chymopapain, and pronase.…”

Section: Introductionmentioning

confidence: 99%

Generation of leukotrienes by purified human lung mast cells.

MacGlashan¹,

Schleimer²,

Peters³

et al. 1982

J. Clin. Invest.

275

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A B S T R A C T Although mediator release from mast cells and basophils plays a central role in the pathogenesis of human allergic disease, biochemical studies have been restricted to rat peritoneal mast cells and basophilic leukemia cells because they could be easily purified. We have used two new techniques of cell separation to purify human lung mast cells to 98% homogeneity. Lung cell suspensions were obtained by dispersion of chopped lung tissue with proteolytic enzymes. Mast cells were then purified from the suspensions by countercurrent centrifugal elutriation and affinity chromatography. The purified mast cells released both histamine and slow-reacting substance of anaphylaxis (SRS-A) (leukotriene C and D) during stimulation with goat anti-human IgE antibody. Moreover, these preparations were able to generate significant quantities of SRS-A (32±7X 10-'7 LTD moleequivalents/mast cell) at all stages of purification, indicating that a secondary cell is not necessary for the antigen-induced release of SRS.

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“…Human isolated lung tissue can be passively sensitized with IgE antibody by incubation in sera from asthmatic patients which contain a relatively high concentration of reaginic antibody. Histamine and slow reacting substance (SRS-A) are known to be released when tissue sensitized in this way is subsequently challenged with the corresponding antigen (Sheard, Killingback & Blair, 1967) and both are bronchoconstrictor in man (Brocklehurst, 1956). Prostaglandin F2a is also broncho-constrictor in man (Sweatman & Collier, 1968) whereas prostaglandins E1 and E2 are bronchodilator (Cuthbert, 1969;Smith & Cuthbert, 1972;Herxheimer & Roetscher, 1971).…”

Section: Introductionmentioning

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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Antigen Induced Release of Histamine and SRS-A from Human Lung passively sensitized with Reaginic Serum

Cited by 114 publications

References 6 publications

Immunological Release of Histamine from Human Lung

Immunological Release of Histamine from Human Lung

Generation of leukotrienes by purified human lung mast cells.

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

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