Cancer and skin sensitivity to intradermal histamine: a preliminary report.
0
Citation
0
Reference
10
Related Paper
Abstract:
Any meaningful relationship of histamine concentrations, serum IgE concentrations, and the prevalence of cancer is unproven. Several reports indicate that tumor growth is associated with an increased synthesis of histamine. Others demonstrate decreased blood histamine levels and reduced cutaneous response to intradermal histamine in patients with solid malignant tumors. We have evaluated skin sensitivity to intradermal histamine injection, and IgE levels in cancer patients either with or without metastasis. Our data reveal no differences for histamine-induced wheal and flare areas between normal subjects and patients with neoplastic disease (with or without metastasis). In addition serum IgE concentrations were not statistically different. Skin sensitivity to intradermal histamine is not decreased in patients with cancer.Keywords:
Intradermal injection
Cite
Histamine-releasing factor or HRF is a collective term used for a heterogeneous group of factors with different modes of action. The current review is focussed on IgE-dependent HRF that require the presence of certain types of IgE (designated IgE+) to induce histamine release. IgE+ might be a structurally different IgE molecule, or, alternatively, autoreactive IgE. A subgroup of IgE-dependent HRF does not bind to IgE, such as cloned HRF p23. This factor turned out to be a basophil-priming cytokine. Alternatively IgE-dependent HRF might be an autoallergen. Several groups demonstrated IgE antibodies to human proteins. However, not all IgE autoallergen-containing extracts induce histamine release of appropriately sensitized basophils. In culture supernatants of human mononuclear cells an autoallergenic activity (Agmn) is found, but no binding to IgE+ was found yet. Agmn might be an autoallergen, since it is cross-reactive with a grass pollen allergen in the stripped basophil assay. IgE-dependent HRF and IgE+ may play a role in the late allergic reaction (LAR). However, IgE+ responsiveness to Agmn (IgEmn+) was not required for a bronchial LAR. IgEmn+ is associated with chronic allergic disease, since the prevalence of IgEmn+ is high in the serum of severe asthmatics and atopic dermatitis patients. Our hypothesis is that exogenous allergens induce IgE antibodies cross-reactive with an endogenous protein. During a LAR, these endogenous proteins are released and the subsequent IgE-mediated reaction prolongs and aggravates the allergic and/or asthmatic symptoms. In conclusion, HRF is a confusing term since it is used for different activities. It might be better to avoid this terminology on and just describe the activity of the factors. Autoallergenic activity is likely to explain most, if not all, IgE-dependent activity.
Priming (agriculture)
Cite
Citations (16)
We studied immunoglobulin E (IgE)- and non-IgE-mediated releasability in basophils from 31 patients with hydatidosis. Histamine release to non-IgE-dependent stimuli did not differ significantly between normal individuals and patients with hydatidosis. On the contrary, an increased histamine liberation was obtained by challenging basophils from hydatid patients with anti-human IgE. It is concluded that <i>Echinococcus granulosus</i> infection induces an enhanced sensitivity of basophils to IgE-dependent stimuli.
Basophil activation
Cite
Citations (3)
Basophil leukocytes obtained from AIDS patients, allergic patients and healthy control were stimulated in vitro with interleukin 4, lymphotoxin, tumour necrosis factor alpha and interferon gamma to examine the histamine releasing effect. The cytokines caused histamine release from the basophils of approximately half the AIDS patients and from 8–17% of the allergic patients. No response was obtained in the control group. Removal of cell surface immunoglobulins abolished the response to cytokines, indicating an Ig‐dependent mechanism. Passive sensitization with cell‐derived Ig, with Ig deprived of IgE, or with IgG, indicated that cell‐bound IgE was responsible for the cytokine‐induced histamine release in AIDS patients. This response may be mediated by cytokine‐selective IgE antibodies.
Cite
Citations (9)
Summary Background Allergen‐specific immunotherapy has proven to be clinically effective in the treatment of patients with atopic asthma; however, the mechanisms are still unclear. Several noted immunological changes include an increase of the allergen‐specific IgG antibody, a reduction in the allergen‐specific IgE antibody subsequent to transient increase, an allergen‐specific T cell shift in cytokine production from Th2 to Th1, and a decrease in quantity and activity of basophils and mast cells. Objective To analyse the changes of basophil histamine release in response to IgE‐mediated and non‐IgE‐mediated stimuli before and after conventional house‐dust mite immunotherapy in children who suffer from atopic asthma. Methods Fourteen Dermatophagoides farinae ( Df ) sensitive asthmatic children with conventional immunotherapy were examined. Basophil histamine releasability was measured 0 months (just before immunotherapy), 4 months and 9 months after immunotherapy. Basophils were stimulated with Df and goat anti‐human IgE antibody as IgE‐mediated stimuli; and formyl‐Met‐Leu‐Phe (fMLP) and calcium ionophore A23187 as non‐IgE‐mediated stimuli. Accordingly, the asthma symptom score was used to assess clinical outcome and the skin test reactivity to Df was measured. Results In contrast to pre‐immunotherapy activity, 4 and 9 months after immunotherapy there were significant decreases in histamine release by Df and by anti‐IgE antibody. The histamine release by fMLP and by calcium ionophore showed no significant changes after immunotherapy. Histamine release by Df demonstrated significant correlation to that by anti‐IgE antibody and by fMLP, yet there was no observable correlation between histamine release by Df and by calcium ionophore. The asthma symptom score decreased significantly 4 and 9 months after immunotherapy and showed significant correlation with histamine release by Df . The skin test reactivity (allergen/histamine ratio) remained constant 4 months after immunotherapy, but decreased significantly 9 months after immunotherapy. Conclusion Basophils have the potential to play an important role in the early clinical improvement of conventional immunotherapy in children with atopic asthma, which may be a result of the decreased IgE‐mediated histamine releasability during immunotherapy.
Allergen Immunotherapy
Cite
Citations (67)
Summary In this study we have examined the relationship between the in vitro basophil histamine‐releasing activity of human IgG anti‐IgE, isolated as euglobulin fractions from sera of asthmatic patients, and its IgG1/IgG4 subclass distribution. In particular, we have investigated whether IgG anti‐IgE modulates allergen‐induced basophil activation. The study has revealed that only a small proportion of IgG anti‐IgE samples triggered histamine release from basophils of an asthmatic individual (4/21; 19%), a hay fever sufferer (4/10; 40%) and a healthy person (7/21; 33%). The basophil histamine‐releasing activity of IgG anti‐IgE did not seem to be determined by the IgG1/IgG4 subclass composition of the IgG anti‐IgE preparation used. Furthermore, we have demonstrated that autoanti‐IgE antibodies modulate allergen‐induced basophil histamine release. The three modulatory effects exerted by IgG anti‐IgE antibodies on allergen‐triggered basophil activation (i.e. additive, synergistic and blocking) were not dependent on the subclass nature of IgG anti‐IgE or the use of histamine‐releasing anti‐IgE preparations. Our data suggest that IgG anti‐IgE antibodies in asthma patients may consist of two functionally distinct subpopulations: those which up‐regulate (pro‐allergic) and those which down‐regulate (anti‐allergic) the allergic release of mediators from mast cells and basophils.
Basophil activation
Cite
Citations (36)
In this study we analysed the presence and proportions of IgE specific for Df 6 and Df 11 two purified allergens of <i>Dermatophagoides farinae</i>. The characterisation of serum IgE and cell-bound IgE for 3 <i>D. farinae</i>-sensitive patients were performed by CRIE, RAST and PRIST assays. Furthermore the basophils from these same patients were studied by histamine release assays in the presence of Df 6 and Df 11. All the individual patient’s cell and serum IgE samples displayed the presence of IgE antibodies specific for Df 6 and Df 11 but the relative quantities of the IgE for these two specificities were characteristic of each patient. The ratios (Specific IgE for Df 11): (Specific IgE for Df 6) (ratio 11:6) were similar in the serum and on the cells for an individual patient. As judged by histamine release assays, the basophil sensitivities towards Df 6 and Df 11 were very different from one atopic patient to another. Moreover cell sensitivities reflected the proportion of Df 6- and Df 11-specific IgE antibodies found in the serum and in the cell eluate.
Cite
Citations (15)
Possible functional heterogeneity of human IgE antibody was studied by passively sensitizing human basophils for antigen-induced histamine release. Six sera of known IgE anti-ragweed antigen E and total IgE content were diluted to contain 10 ng of antibody but differed with respect to the ratio of specific/total IgE. The relative ability of the sera to passively sensitize generally reflected the specific/total IgE ratio but one serum was 2.5 times more active than the remainder. This ability did not reflect the IgG antibody level nor was it due to a dialyzable or heat-stable factor. These data indicate functional IgE heterogeneity, probably due to the interaction of the Fc portion of IgE with the basophil receptor.
Cite
Citations (26)
Parasite-specific IgE levels correlate with human resistance to reinfection with Schistosoma spp. after chemotherapy. Although the role of eosinophils in schistosomiasis has been the focus of a great deal of important research, the involvement of other Fcε receptor-bearing cells, such as mast cells and basophils, has not been investigated in relation to human immunity to schistosomes. Chemotherapy with praziquantel (PZQ) kills schistosomes living in an in vivo blood environment rich in IgE, eosinophils and basophils. This releases parasite Ags that have the potential to cross-link cell-bound IgE. However, systemic hypersensitivity reactions are not induced by treatment. Here, we describe the effects of schistosomiasis, and its treatment, on human basophil function by following changes in total cellular histamine and in vitro histamine-release induced by schistosome Ags or anti-IgE, in blood samples from infected Ugandan fishermen, who are continuously exposed to S. mansoni infection, before and 1-day and 21-days after PZQ treatment. There was a significant increase in the total cellular histamine in blood samples at 1-day post-treatment, followed by a very significant further increase by 21-days post-treatment. In vitro histamine-release induced by S. mansoni egg (SEA) or worm (SWA) Ags or anti-IgE antibody, was significantly reduced 1-day post-treatment. The degree of this reduction correlated with pre-treatment infection intensity. Twenty-1-days post-treatment, SEA-induced histamine-release was still significantly lower than at pretreatment. Histamine-release was not correlated to plasma concentrations of total or parasite-specific IgE, nor to specific IgG4 plasma concentrations. The biology of human blood basophils is modulated by S. mansoni infection and praziquantel treatment. Infection intensity-dependent suppression of basophil histamine-release, histamine-dependent resistance to infection, and similarities with allergen desensitisation are discussed as possible explanations of these observations.
Cite
Citations (22)
Experiments were done to clarify the mechanisms associated with releasability of histamine. First, washed leukocytes from 23 asthmatic patients sensitive to mite allergen were challenged with Der p 1, a major allergen isolated from Dermatophagoides pteronyssinus , or anti‐IgE. A significant correlation was observed between the ratio of Der p 1‐specific IgE liter to total IgE level (S/T) in the patient's plasma and either the reactivity (maximal percentage of histamine release; r s = 0.514, P = 0.016, n = 23) or the sensitivity (the minimum allergen concentration required to achieve 25% histamine release; r s = ‐0.790, P = 0.0002) to Der p 1. Additionally, the reactivity to Der p 1 was significantly correlated with that to anti‐IgE (r s = 0.690, P = 0.0012), indicating that an intrinsic cellular property may be one of the contributing factors in immunologic histamine release. In a second series of experiments, sinus mast cells were passively sensitized with immunoglobulins prepared from the patient's plasma. A statistically significant correlation was found between either the reactivity or the sensitivity to Der p 1 and S/T, thus indicating that S/T is an indicator of the releasability of histamine. When basophils or mast cells were passively sensitized with mouse IgE and subsequently stimulated with antimouse IgE, the reactivity to antihuman IgE was significantly correlated with that to antimouse IgE ( r s = 0.966, P = 0.0023, n = 11). These observations suggest that an intrinsic cellular property regulates reactivity in immunologic histamine release. Taken together, our results suggest that an intrinsic cellular property, as well as specific IgE antibody levels on the cell surface, is an important factor in determining histamine release in response to IgE‐dependent activation.
Basophil activation
Cite
Citations (10)
Incubation of airways from nonatopic patients with serum from patients with high IgE levels confers responsiveness to "specific" (allergen) and hyperresponsiveness to "nonspecific" (histamine) stimuli. We have tested the hypothesis that the level of IgE determines the degree of specific and nonspecific responsiveness. Bronchial rings from nonatopic patients were sensitized overnight with serum containing high levels of allergen-specific IgE, or with an allergen-specific chimeric IgE (JW8) in physiologic buffer. In vitro responsiveness to allergen and histamine was evaluated and compared with non-sensitized tissues from the same patients. Responses to specific allergen were demonstrated in all tissues sensitized with atopic serum or chimeric IgE, but not in nonsensitized tissues. Allergen responses were specific, since tissues sensitized using serum containing high Dermatohagoides farinae-specific IgE only, did not respond to either horse or dog allergens. The potency and magnitude of the maximal contraction to histamine was significantly (p < 0.05) increased in tissues sensitized using atopic serum with high total IgE concentrations compared with nonsensitized preparations, but was unchanged in tissues sensitized using chimeric IgE or serum with low total IgE levels. Therefore, specific IgE determines allergen responsiveness in passively sensitized human airways, but histamine hyperresponsiveness is independent of specific IgE and appears to be related to some other factor associated with serum containing high concentrations of total IgE.
Cite
Citations (63)