Release of Mast-Cell Mediators and Alterations in Lung Function in Patients with Cholinergic Urticaria

Soter, Nicholas A.; Si, Wasserman; Austen, K. Frank; Er, McFadden

doi:10.1056/nejm198003133021104

Cited by 150 publications

(42 citation statements)

References 28 publications

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“…Reed and associates nioted a simiiilar pheniomiienioni in humans and were unable to find mleasurable chaniges in circulating histamiinle with anitigeni challenges. 3 We do not believe that our inability to detect histamnine in this study is the result of technical problemns with the assay incasmiiuch as we have previously measuired the release kinetics of this molecule in patients with idiopathic cold-indluced urticaria (10,11), cholinergic urticaria (24), and idiopathic solar urticaria (23). One explanationi for these apparenit discrepancies is that although it is possible to meeasure histamine in a local circulation, dlraining an experimentally challenged site, such as the skini, it may well be that its rapid metabolismn precludes detectioni of' appreciable (quiantities at sites far remoxed from the originial reaction.…”

Section: Methodsmentioning

confidence: 80%

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Evaluation of Role Played by Mediators of Immediate Hypersensitivity in Exercise-induced Asthma

Deal¹,

Wasserman²,

Soter³

et al. 1980

J. Clin. Invest.

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129

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A B S T R A C T To (letermiiine whether mnediators ofimmnediate hypersensitivity played a role in the pathogenesis of exercise-induced asthma, we measured the concentration of histamine and neutrophil-chemotactic activity present in systemic arterial blood during thermal challenges in five asymptomatic asthmatics. Because exercise-induced asthma has been shown to be a result of respiratory heat loss and because respiratorv heat loss during isocapnic hyperventilation has been shown to give identical responses, we chose the latter provocational method in order to minimllize increases in cardiac output that might interfere with the interpretation of mediator concentrations in arterial blood. Multiple aspects of pulmonarv mechanics were also recorded before and after provocation. The results of these studies were then compared with the effects observed when the same subjects inhaled aerosols of specific antigens on the same day. Each challenge produced identical alterations in lung function, and neither was associated with consistent changes in arterial histamine. However, antigen provocation evoked a sustained and prolonged release of neutrophil chemotactic activity in each subject, whereas isocapnic hyperventilation with cold air was without effect. These data strongly suggest that mast-cell derived mediators are not involved in the development or mainitenance of the bronchial obstruction that follows exercise in asthmatics.

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Section: Methodsmentioning

confidence: 80%

“…Ouir observations form the basis of'this report. Chemnotaxis was assessed by' a modification (19) of the Bov'den chamiber assav (20) (Ig)E mast-cell mediated disorders (10,11,23,24). Thus, although the molecular weight of the presently described molecule is not yet known, its release kinetics suggest that the likely source is from the mast cell.…”

mentioning

confidence: 99%

Evaluation of Role Played by Mediators of Immediate Hypersensitivity in Exercise-induced Asthma

Deal¹,

Wasserman²,

Soter³

et al. 1980

J. Clin. Invest.

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129

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“…Comparable NCF have been identified in the sera from cold (2), cholinergic (3), and solar (4) urticaria after the appropriate challenge. There is circumstantial evidence to suggest that NCF might be derived from the mast cell.…”

Section: Introductionmentioning

confidence: 99%

Identification and partial characterization of an exercise-induced neutrophil chemotactic factor in bronchial asthma.

Lee¹,

Nagy²,

Nagakura³

et al. 1982

J. Clin. Invest.

186

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A B S T R A C T A heat-stable neutrophil chemotactic factor (NCF) has been identified in the serum of 13 atopic asthmatic subjects after treadmill exercise. Peak activity was detected at 10 min and returned to prechallenge values by 1 h. No NCF activity was detected in the sera of three nonasthmatic atopic or four normal nonatopic individuals performing the same task. NCF produced by exercise (NCFEX) had a similar timecourse of release to NCF provoked by specific antigen (NCFAG). The appearance of circulating NCFEX and NCFAG closely paralleled the fall in peak expiratory flow rate/forced expiratory volume in 1 s (PEFR/ FEVI). Histamine challenge in atopic asthmatics at concentrations giving a comparable change in PEFR/ FEVy to that evoked by exercise or inhaled antigen was not associated with the appearance of circulating NCF. In seven subjects NCFEX release was inhibited by prior administration of disodium cromoglycate. NCFEX and NCFAG eluted as single peaks of activity when applied separately to columns of Sephadex G-200, and both were an estimated 750,000 daltons. NCFEX and NCFAG also eluted as single peaks of activity, at between 0.15 and 0.30 M NaCl, following anion exchange chromatography on DEAE-Sephacel (pH 7.8). The isoelectric points of NCFEX and NCFAG were virtually identical (between pH 6.0 and 6.5) as determined by chromatofocusing on Polybuffer Exchanger 94. The activities of NCFEx and NCFAG were substantially reduced, in both a time-and dose-dependent fashion, after incubation with trypsin and chymotrypsin. Partially purified NCFEX and NCFAG promoted both stimulated random migration (chemokinesis) as well as directional migration (chemotaxis).These experiments indicate that NCFEX and NCFAG might be identical substances and raise the possibility

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“…The cell pellet was resuspended in 1 ml reaction buffer and sonicated. Histamine in sonicated cell pellet and supernatant was assessed by a sensitive radioenzymatic method [3]. Release of histamine is calculated as: stimulated releasespontaneous release residual histamine + released histaminespontaneous release Net percentage release of histamine is calculated as percent release with drug -percent release in buffer alone.…”

Section: Methodsmentioning

confidence: 99%

Anaphylactic reaction to cytarabine: In vitro evidence that the response is immunoglobulin e mediated

Markman

Howell

King

et al. 1984

Med. Pediatr. Oncol.

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A 48-year-old female developed significant bronchospasm on two occasions after being treated with cytarabine (Ara-C) by the intraperitoneal route. In this report we present the first in vitro evidence that such a reaction to cytarabine can be associated with the release of histamine and therefore might be immunoglobulin E (IgE) mediated. In addition, this report emphasizes the fact that, while uncommon, severe allergic reactions to this useful chemotherapeutic agent do occur and must be considered in the differential diagnosis of anaphylaxis and related symptoms in patients receiving this drug.

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Release of Mast-Cell Mediators and Alterations in Lung Function in Patients with Cholinergic Urticaria

Cited by 150 publications

References 28 publications

Evaluation of Role Played by Mediators of Immediate Hypersensitivity in Exercise-induced Asthma

Evaluation of Role Played by Mediators of Immediate Hypersensitivity in Exercise-induced Asthma

Identification and partial characterization of an exercise-induced neutrophil chemotactic factor in bronchial asthma.

Anaphylactic reaction to cytarabine: In vitro evidence that the response is immunoglobulin e mediated

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