Enhanced basophil histamine release to concanavalin A in allergic rhinitis

Busse, William W.; Swenson, Cheri A.; Sharpe, Geralyn; Koschat, Martin A.

doi:10.1016/0091-6749(86)90119-3

Cited by 32 publications

(22 citation statements)

References 14 publications

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“…But these observations suggest that the linkage between basophil function and disease response to omalizumab is possibly different from the linkage between the basophil response and disease severity. The linkage between basophil response and disease severity is not strong 33–39 . For treatment to reveal that the change in basophil response has an influence on the efficacy of treatment suggests there are other factors involved.…”

Section: Discussionmentioning

confidence: 99%

Omalizumab increases the intrinsic sensitivity of human basophils to IgE-mediated stimulation

MacGlashan

Saini

2013

Journal of Allergy and Clinical Immunology

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Background Treatment of allergic patients with omalizumab results in a paradoxical increase in their basophil histamine release response, ex vivo, to crosslinking anti-IgE antibody. It is not known whether this change in response is associated with an increase in intrinsic cellular sensitivity, which would be a paradoxical response. Objective To determine if the increase in response to anti-IgE Ab is a reflection of an increased cellular sensitivity, expressed as molecules of antigen-specific IgE per basophil required to produce a 50% of maximal response. Methods Patients were treated with omalizumab or placebo agent for 12 weeks (NCT01003301 at ClinicalTrials.gov) and the metric of basophil sensitivity was assessed at 4 time points, baseline, 6–8 weeks, 12 weeks (after which treatment stopped) and 24 weeks (12 weeks after the end of treatment). Results As observed previously, treatment with omalizumab resulted in a marked increase in the maximal histamine release induced by crosslinking anti-IgE Ab. This change was accompanied by a marked shift in intrinsic basophil sensitivity, ranging from 2.5 to 125 fold, with an average of 6 fold at the midpoint of the treatment to 12 fold after 12 weeks. The magnitude of the increase in cellular sensitivity was inversely related to the starting sensitivity or the starting maximum histamine release. The increased cellular sensitivity also occurred when using LTC4 secretion as a metric of the basophil response. 12 weeks after the end of treatment, cellular sensitivity was found to shift towards the baseline level although the return to baseline was not yet complete at this time point. Conclusions Treatment with omalizumab results in a markedly increased sensitivity of basophils to IgE-mediated stimulation, in terms of the number of IgE molecules required to produce a given response. These results provide a better quantitative sense of the phenotypic change that occurs in basophils during omalizumab treatment which has implications both mechanistic and clinical.

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Section: Discussionmentioning

confidence: 99%

Omalizumab increases the intrinsic sensitivity of human basophils to IgE-mediated stimulation

MacGlashan

Saini

2013

Journal of Allergy and Clinical Immunology

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“…Limited studies have implicated basophils in the development of AR. Basophils have been demonstrated in nasal washes of patients with allergic rhinitis (25–27). …”

Section: Introductionmentioning

confidence: 99%

Sequential Engagement of FcεRI on Mast Cells and Basophil Histamine H4 Receptor and FcεRI in Allergic Rhinitis

Shiraishi

Jia

Domenico

et al. 2013

The Journal of Immunology

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Histamine H4 receptor (H4R)-deficient mice (H4R−/−), H4R antagonist-treated WT mice, and WT mice depleted of basophils failed to develop early (EPR) or late phase (LPR) nasal responses following allergen sensitization and challenge. Basophil transfer from WT but not H4R−/− mice restored the EPR and LPR in H4R−/− mice. Following passive sensitization with OVA-specific IgE, FcεRI−/− recipients of WT basophils plus OVA and histamine developed an EPR and LPR. OVA-IgE passively sensitized FcεRI−/− recipients of H4R−/− basophils and OVA and histamine challenge failed to develop an EPR or LPR, and basophils were not detected in nasal tissue. In contrast, recipients of basophils from IL-13−/− and IL-4−/−/IL-13−/− mice developed an EPR but not LPR. These results demonstrate the development of allergic rhinitis proceeded in two distinct stages: histamine release from FcεRI-activated mast cells, followed by histamine-mediated recruitment of H4R-expressing basophils to the nasal cavity and activation through FcεRI.

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“…On the other hand, it has been shown that lectins can stimulate mast cells and basophils of mammalian species to release histamine [5][6][7][8]. Siraganian and Siraganian [5] have shown that the basophil histamine release (HR) in duced by concanavalin A (Con A) has a great similarity with the immunological release by allergens or anti-IgE, but that the reaction is inhibited by sugars, such as a-mcthyl-D-mannoside or glucose, suggesting that the lec tin-induced HR is based on the interaction with the carbo hydrate component on the Fc region of IgE.…”

Section: Introductionmentioning

confidence: 99%

Interaction of Lectins with Human IgE: IgE-Binding Property and Histamine-Releasing Activity of Twelve Plant Lectins

Shibasaki

Sumazaki

Isoyama

et al. 1992

Int Arch Allergy Immunol

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We examined the IgE-binding reaction and the histamine-releasing response of basophils to a panel of 12 lectins: concanavalin A (Con A), Lens culinaris hemagglutinin (LcH), Pisum sativum agglutinin (PSA), wheat germ agglutinin (WGA), soybean agglutinin (SBA), Bauhinia purpurea agglutinin (BPA), peanut agglutinin (PNA), Ricinus communis agglutinin I (RCA-I), Lotus tetragonolobus agglutinin (Lotus A), Ulex europeus agglutinin I (UEA-I), phytohemagglutinin E (PHA-E) and phytohemagglutinin L (PHA-L). IgE from allergic patients bound with high affinity to Con A, LcH, PSA, RCA-I and PHA-E, and with lower affinity to WGA, BPA, Lotus A and UEA-I, but they did not bind to SBA, PNA or PHA-L. There was no apparent individual difference in the reactivity of IgE to these lectins between 10 IgE preparations from allergic patients. The binding to these lectins, except Lotus A and UEA-I, were competitively inhibited by the lectin-specific sugars or glycopeptide. Upon stimulation by Con A, LcH, PSA, WGA, RCA-1 and PHA-E, leukocytes from allergic patients showed a significant release of histamine, but cells from IgE-deficient subjects did not respond to these lectins. The histamine-releasing responses by these lectins were also inhibited by specific sugars or glycopeptides.

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Enhanced basophil histamine release to concanavalin A in allergic rhinitis

Cited by 32 publications

References 14 publications

Omalizumab increases the intrinsic sensitivity of human basophils to IgE-mediated stimulation

Omalizumab increases the intrinsic sensitivity of human basophils to IgE-mediated stimulation

Sequential Engagement of FcεRI on Mast Cells and Basophil Histamine H4 Receptor and FcεRI in Allergic Rhinitis

Interaction of Lectins with Human IgE: IgE-Binding Property and Histamine-Releasing Activity of Twelve Plant Lectins

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