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PubMed1997

Mast cell involvement in gastritis with or without Helicobacter pylori infection.

BACKGROUND & AIMS: Mast cells are initiators and regulators of inflammation, but their role in the human stomach remains unclear. Therefore, the extent and distribution of mast cell involvement in gastritis with or without Helicobacter pylori infection was investigated. METHODS: Mapped biopsy specimens from 17 H. pylori-positive and 20 H. pylori-negative subjects were examined. Sections were assessed for infection and inflammation and stained with anti-human mast cell tryptase to count mucosal and epithelial mast cells. Density of mast cells in different gastric compartments, their response to infection treatment, and their relationship with other inflammatory cells were evaluated. Mast cell degranulation was evaluated by electron microscopy. RESULTS: Mast cell density was significantly greater in the mucosa with gastritis, with or without H. pylori infection, than in the mucosa of noninfected normal subjects. In the antrum, density was much greater in H. pylori-infected peptic ulcer subjects than in the other gastritis groups. It also correlated significantly with the intensity of inflammation. Mast cell degranulation was demonstrated by electron microscopy in H. pylori-infected mucosa. Mast cell density in ulcer patients decreased significantly after cure of H. pylori infection. CONCLUSIONS: Mast cells may be important effector cells in the pathogenesis of gastritis, especially in H. pylori-associated peptic ulcer.

Adult↗
PubMed2002

Protease-activated receptor-2 (PAR-2) in the pancreas and parotid gland: Immunolocalization and involvement of nitric oxide in the evoked amylase secretion.

Protease-activated receptor-2, a G protein-coupled receptor activated by serine proteases such as trypsin, tryptase and coagulation factors VIIa and Xa, modulates pancreatic and salivary exocrine secretion. In the present study, we examined the distribution of PAR-2 in the pancreas and parotid gland, and characterized the PAR-2-mediated secretion of amylase by these tissues in vivo. Immunohistochemical analyses using the polyclonal antibody against rat PAR-2 clearly showed abundant expression of PAR-2 in rat pancreatic and parotid acini. The PAR-2 agonist SLIGRL-NH2, administered intraperitoneally (i.p.) at 1-10 micromol/kg and 1.5-15 micromol/kg, in combination with amastatin, an aminopeptidase inhibitor, facilitated in vivo secretion of pancreatic and salivary amylase in a dose-dependent manner, respectively, in the mouse. The PAR-2-mediated secretion of pancreatic amylase was abolished by pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor. The secretion of salivary amylase in response to the PAR-2 agonist at a large dose, 15 micromol/kg, but not at a smaller dose, 5 micromol/kg, was partially reduced by L-NAME. Pretreatment with capsaicin for ablation of the sensory neurons did not modify the PAR-2-mediated secretion of pancreatic and salivary amylase in the mouse. In conclusion, our study demonstrates expression of PAR-2 in rat pancreatic acini as well as parotid acini and indicates that nitric oxide participates in the PAR-2-mediated in vivo secretion of pancreatic amylase, and, to a certain extent, of salivary amylase, although capsaicin-sensitive sensory neurons, known to be activated by PAR-2, are not involved in the evoked pancreatic or salivary amylase secretion.

Amino Acid Sequence↗
PubMed1999

Effects of daphnodorin A, daphnodorin B and daphnodorin C on human chymase-dependent angiotensin II formation.

We investigated whether daphnodorin A, daphnodorin B and daphnodorin C inhibited human chymase-dependent angiotensin II-forming activity. Although the structures of these compounds are very similar, daphnodorin A completely inhibited angiotensin II formation generated by chymase, while daphnodorin B partially inhibited and daphnodorin C did not. On the other hand, these daphnodorins did not affect angiotensin converting enzyme-dependent angiotensin II formation. Furthermore, these daphnodorins did not inhibit purified human tryptase, which, like chymase, is contained in mast cells. Therefore, daphnodorin A, but not daphnodorin B and daphnodorin C, may specifically inhibit the chymase-dependent angiotensin II formation, and such differences between inhibitory effects of these compounds to human chymase may be useful for the development of human chymase inhibitor.

Adult↗
PubMed1994

Increased plasma calcitonin levels in systemic mast cell disease.

Aspirin therapy for patients with systemic mast cell disease (SMCD) decreases the production of prostaglandin D2, which is thought to be a major mediator of flushing. Paradoxically, in 5 to 10% of patients with SMCD, administration of aspirin causes massive mediator release and an anaphylactoid reaction. We attempted aspirin desensitization in a 34-year-old man with SMCD (confirmed by bone marrow biopsy) who was incapacitated by severe flushing episodes and hypotension. His baseline mediator levels of plasma calcitonin, urinary histamine, and urinary N-methyl-imidazoleacetic acid were abnormal. Pentagastrin stimulation increased the plasma level of calcitonin from 47 pg/mL to 130 pg/mL (normal, less than or equal to 110) at 5 minutes. Oral aspirin desensitization was begun; however, after a cumulative dose of 620 mg, an anaphylactoid reaction ensued in conjunction with hypotension, abdominal cramping, and flushing. Coincidentally, 1 hour after the episode, the plasma calcitonin level increased from 37 pg/mL to 540 pg/mL, and the serum tryptase level increased from 1 ng/mL to 3.9 ng/mL. Six hours after the episode, the urine level of histamine increased from 90 micrograms/g creatinine to 337 micrograms/g creatinine, and the urinary N-methylimidazoleacetic acid increased from 32 mg/24 h to 81 mg/24 h. Hence, the patient had increased basal levels of plasma calcitonin that increased substantially during aspirin desensitization and increased to above the upper limit of normal during pentagastrin stimulation. Human mast cells may be capable of producing calcitonin or causing secretion of calcitonin in response to skeletal changes.

Adult↗
PubMed1997

The potential role of mast cells in lung allograft rejection.

To perform a retrospective pilot study of the potential role of mast cells in acute and chronic rejection of the lung allograft, transbronchial biopsies of 29 patients with acute rejection and six patients with bronchiolitis obliterans were stained with antibodies to mast cell tryptase. The number of mast cells per unit area were counted, and compared with a control group of normal lung biopsies stained in a similar fashion. Increasing grades of acute rejection were associated with progressively more mast cells per high-power microscopic field. The presence of bronchiolitis obliterans was accompanied by the greatest numbers of mast cells. Mast cells may play a role in the acute rejection response to the lung allograft and in the development of bronchiolitis obliterans.

Aged↗
PubMed2001

Biopsy features are associated with primary symptoms in interstitial cystitis: results from the interstitial cystitis database study.

The purpose of this study was to investigate associations between bladder biopsy features and urinary symptoms for patients enrolled in the Interstitial Cystitis Database (ICDB) Study. Bladder biopsies were obtained during baseline screening in the ICDB Study and were evaluated for histopathologic features. Multivariable models for nighttime voiding frequency, urinary urgency, and pain were developed, incorporating biopsy features from the most diseased area of the bladder as predictors, adjusting for significant clinical factors, and clinical center variation. Among 204 interstitial cystitis (IC) patients providing biopsy specimens, cystoscopic pathology findings were not statistically associated (P >0.1) with primary IC symptoms, although the presence of Hunner's ulcer (n = 12) was suggestive of increased urinary frequency. Within a multivariable predictive model for nighttime voiding frequency, adjusting for age and minimum volume per void, 4 pathology features were noted: (1) mast cell count in lamina propria on tryptase stain; (2) complete loss of urothelium; (3) granulation tissue in lamina propria; and (4) vascular density in lamina propria on factor VIII (F8) stain were statistically significant (P <0.01). Similarly, in a multivariable model for urinary urgency, minimum volume, and percentage of submucosal granulation tissue remained statistically significant (P <0.01). Finally, the percentage of mucosa denuded of urothelium and the percentage of submucosal hemorrhage remained highly associated (P <0.01) with pain in a multivariable predictive model. The fact that the presence or severity of glomerulations was not selected for any of these predictive models suggests that cystoscopic findings of glomerulations are not predictive of IC symptoms. Furthermore, these results suggest an important role for certain pathologic features in the predictive modeling of IC symptoms.

Analysis of Variance↗
PubMed2002

Leukocyte populations in interstitial cystitis and idiopathic reduced bladder storage.

OBJECTIVES: Mast cells and leukocyte populations in bladder biopsies from women with interstitial cystitis (IC) or idiopathic reduced bladder storage (sensory urgency [SU]) were compared to determine whether any evidence of a common etiology between these conditions could be found. METHODS: Biopsies from 40 patients (9 meeting the National Institute of Arthritis, Diabetes, Digestive and Kidney Diseases criteria [IC] and 31 who did not [SU]) and 20 controls (having colposuspension for stress incontinence) were stained with monoclonal antibodies against leukocyte antigens and mast cell tryptase. The median cell counts from 10 high power fields were calculated and compared between cases and controls. The clinical and urodynamic data were also compared. RESULTS: Nocturia (odds ratio 26.7; 95% confidence interval 3.3 to 245.5) and bladder pain (odds ratio 18.5; 95% confidence interval 1.8 to 193.1) were associated with significant odds ratios for disease (IC or SU compared with controls) in logistic regression analysis. Patients with IC were significantly older than those with SU (P = 0.05). Leukocyte populations showed only increased CD20+ cells in patients with IC compared with the others (P = 0.03). CONCLUSIONS: The analysis of the clinical, urodynamic, and cystoscopic data showed no differences between patients with IC and those with SU, except for age. Nocturia or bladder pain discriminated between patients and controls. The lymphocytic infiltrate in SU is similar to that seen in IC but with fewer CD20+ cells. These data support the work of others and may indicate that SU has a common etiology with IC.

Case-Control Studies↗
PubMed1998

Altered expression of bladder mast cell growth factor receptor (c-kit) in interstitial cystitis.

OBJECTIVES: To investigate the presence of mast cell growth factor receptors (c-kit) on bladder mast cells in interstitial cystitis (IC), a bladder condition occurring primarily in women. IC is characterized by pain, urgency, frequency, and mucosal microhemorrhages discernible with cystoscopy under general anesthesia. One of the prevailing theories to explain IC pathophysiology is the increased number of bladder mast cells, many of which are activated in at least a subgroup of IC patients. Stem cell factor (SCF), also known as c-kit ligand, is now recognized as the key molecule responsible for mast cell proliferation and is known to exert its action through specific surface receptors. METHODS: Bladder specimens from patients with IC, identified by the criteria established by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and control patients were obtained during diagnostic cystoscopy and were immediately fixed in 4% paraformaldehyde. They were then examined by immunohistochemistry for the unique proteolytic mast cell enzyme tryptase or the presence of c-kit, or both. RESULTS: Bladders of IC patients contained a higher number of mast cells than control patients. However, mast cells in IC patients expressed fewer c-kit on their surface than those in control patients. These results could be explained if the c-kit were occupied by endogenous SCF or were downregulated, possibly by internalization after ligand-receptor interactions, making them inaccessible to immunocytochemical detection. CONCLUSIONS: Bladder mastocytosis and/or activation of mast cells, in at least a subpopulation of IC patients, may be explained by increased stimulation of mast cells by SCF. These results could be explained either by a mutation leading to constitutive activation of c-kit or overproduction of c-kit ligand leading to bladder mast cell proliferation in IC.

Adolescent↗
PubMed2000

Basophils, eosinophils, and mast cells in atopic and nonatopic asthma and in late-phase allergic reactions in the lung and skin.

BACKGROUND: Previous studies used indirect methods to identify basophils in the bronchi in asthma, and the numbers were not compared with eosinophils and mast cells. Furthermore, differences in basophil numbers between atopic and nonatopic asthma at baseline and between late-phase skin and asthmatic reactions have not been previously documented. OBJECTIVE: The basophil granule-specific mAb BB1 was used to identify basophils in (1) bronchial biopsy specimens from atopic asthmatic subjects and nonatopic asthmatic subjects and control subjects, (2) biopsy specimens from atopic asthmatic subjects before and after inhalational allergen challenge, and (3) late-phase skin reactions. Basophil numbers were compared with EG2(+) eosinophils and tryptase(+) mast cells. METHODS: Cells were enumerated in bronchial and skin biopsy specimens by means of immunohistochemistry with the alkaline phosphatase-antialkaline phosphatase method. RESULTS: There were elevated numbers of basophils in baseline biopsy specimens in atopic asthmatic subjects compared with atopic control subjects or normal control subjects, although eosinophils and mast cells were 10-fold higher. There was an intermediate number of basophils in nonatopic asthmatic subjects. Basophils increased after allergen inhalation, but again basophils were less than 10% of eosinophils. In contrast, basophils in cutaneous late-phase reactions were approximately 40% of infiltrating eosinophils. The peak of basophil accumulation was at 24 hours, whereas maximal eosinophil infiltration occurred at 6 hours. One third of cutaneous basophils had morphologic appearances suggestive of degranulation. CONCLUSION: Numerous basophils infiltrated cutaneous late-phase reactions in atopic subjects. However, this cell was not prominent in bronchial biopsy specimens of asthmatic subjects, either at baseline or after allergen challenge.

Adult↗
PubMed2003

5-oxo-6,8,11,14-eicosatetraenoic acid induces the infiltration of granulocytes into human skin.

BACKGROUND: 5-Oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE) is an arachidonic acid metabolite with potent in vitro chemoattractant effects on eosinophils and neutrophils. It has also been shown to induce pulmonary eosinophilia in Brown Norway rats, but it is not known whether it is active in human beings in vivo. OBJECTIVE: To determine whether 5-oxo-ETE can induce cellular infiltration in patients with atopic asthma and nonatopic control subjects after intradermal administration. METHODS: 5-Oxo-ETE was administered intradermally to 11 patients with atopic asthma and 10 nonatopic control subjects. Skin biopsy specimens were taken 6 or 24 hours later and examined by immunocytochemistry for cells expressing specific markers for eosinophils (major basic protein), neutrophils (elastase), macrophages (CD68), lymphocytes (CD3), and mast cells (tryptase). RESULTS: 5-Oxo-ETE (1.5 and 5 microg) elicited the infiltration of both eosinophils and neutrophils into the skin in both control and atopic asthmatic subjects. Increased numbers of eosinophils were observed at 6 and 24 hours after injection, whereas significantly elevated neutrophil numbers were present only after 24 hours. Eosinophils were >3 times higher in patients with atopic asthma compared with control subjects after injection of the highest dose of 5-oxo-ETE. Macrophage numbers were also elevated, but only at the highest dose of 5-oxo-ETE. No effects were observed on the numbers of either lymphocytes or mast cells. CONCLUSIONS: 5-Oxo-ETE elicits the infiltration of eosinophils and neutrophils into the skin of human beings in vivo after intradermal administration. Asthmatic subjects are more responsive to this substance than nonallergic control subjects. These results suggest that 5-oxo-ETE may be an important mediator of inflammation.

Arachidonic Acids↗
PubMed1992

Exercise-induced asthma is not associated with mast cell activation or airway inflammation.

Exercise-induced asthma (EIA) may affect up to 90% of patients with asthma. Hyperpnea associated with exercise leads to increased airway water and heat loss, which contributes to the development of EIA. Measurement of circulating mediators has suggested that mast cells may participate in the development of EIA via release of histamine and neutrophil chemotactic factor. To evaluate further the contribution of pulmonary mast cell-mediator release in the pathogenesis of EIA and to determine whether EIA is associated with enhancement of airway inflammation, we studied 11 subjects with mild stable asthma (FEV1, 93% +/- 3% predicted; mean +/- SEM) with significant EIA (after exercise fall in FEV1, 41% +/- 5%). Bronchoalveolar lavage (BAL) was performed immediately (less than 1 hour) after exercise challenge (EC) and repeated 24 hours later (exercise studies). On another occasion, paired BALs were done 24 hours apart (control studies). A minimum of 2 weeks separated the exercise and control pairs. No changes were observed in BAL cell counts, differentials, or reactive oxygen species metabolism after EC. Neither BAL histamine nor BAL tryptase levels increased, either shortly (less than 1 hour) or 24 hours after EC. We conclude that EC in subjects with asthma is not associated with cellular influx to airspace and that mechanisms other than histamine release by pulmonary mast cells may be responsible for EIA.

Adolescent↗
PubMed1995

Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation.

To infer possible mechanisms of acute airway inflammation and mucus hypersecretion in acute severe asthma, we performed cellular and biochemical analysis on sputum from 18 adults with acute severe asthma and compared the results with results of analysis of sputum from 12 adults with cystic fibrosis (CF). We found that in subjects with asthma neutrophils made up more than 75% of sputum cells in 10 samples whereas eosinophils made up more than 75% of cells in only three samples. Fifty percent of the subjects with asthma reported that their asthma exacerbation was precipitated by a respiratory tract infection, and these subjects had a significantly higher percentage of neutrophils in their sputum (85% +/- 6% vs 57% +/- 12%, p = 0.05). In the CF samples neutrophils made up more than 95% and eosinophils less than 1% of cells in all samples analyzed. Analysis of fluid phase chemicals in asthmatic and CF sputum samples showed that despite overall lower mean values of neutrophil elastase (27 +/- 11 micrograms/ml vs 466 +/- 121 micrograms/ml, p = 0.0001) and interleukin-8 (IL-8) (55 +/- 15 ng/ml vs 186 +/- 24 ng/ml, p = 0.0001), some of the asthmatic samples had values for these variables that overlapped those in the CF samples. In addition, the asthmatic samples were distinguished by the presence of higher tryptase (10 +/- 7 U/L vs 0.9 +/- 0.9 U/L, p = 0.0001) and interleukin-6 (1166 +/- 447 ng/ml vs 186 +/- 24 ng/ml; p = 0.0001) levels and by a higher ratio of albumin to mucin-like glycoprotein (0.8 +/- 0.5 vs 0.1 +/- 0.002, p = 0.02). DNA levels were lower in the asthmatic samples (0.5 +/- 0.3 mg/ml vs 3.5 +/- 1.2 mg/ml, p = 0.05). We conclude that neutrophils predominate more frequently than eosinophils as the major inflammatory cell in sputum from patients with asthma in acute exacerbation. We speculate that this may be because respiratory tract infections are a frequent precipitant of acute asthma. In addition, the high IL-8 levels and free neutrophil elastase activity observed in asthmatic sputum suggests that IL-8 may mediate airway neutrophilia in acute asthma and that neutrophil elastase may mediate mucin glycoprotein hypersecretion in acute asthma, as has been proposed for the mucin hypersecretion in CF.

Adolescent↗
PubMed1995

Quantitation of inflammatory cells in the nasal mucosa of patients with allergic rhinitis and normal subjects.

BACKGROUND: The role of inflammatory cells at the local site of allergic inflammation in the nose is unclear. METHODS: Nasal biopsy specimens were obtained from 10 patients with symptomatic seasonal allergic rhinitis and 10 normal subjects. Freeze-dried paraffin-embedded sections were stained for mononuclear cells and eosinophils. Tissues in Carnoy's fixative were stained for mast cells. RESULTS: T cells were much more plentiful than B cells or macrophages, and no significant differences were found between the two groups in the number of T cells, T-cell subsets, B cells, and macrophages. However, the number of CD25+ cells (lymphocyte activation markers) and the number of eosinophils were significantly higher in the allergic group than in the control group. There were no significant differences between the two groups in the total mast cell number. However, mucosal type mast cells were slightly increased, and a higher ratio of mast cells were costained for IgE in the allergic group. IgE+ cells mostly constained for mast cell tryptase and did not costain for J chain. CONCLUSIONS: These data suggest that unlike granulocytes, in some mononuclear cells qualitative, not quantitative, changes may be important in allergic rhinitis and that IgE may not be locally produced in the nasal mucosa.

Adult↗
PubMed1996

Effects of cyclosporin A and FK-506 on stem cell factor-induced histamine secretion and growth of human mast cells.

Stem cell factor (SCF) is a key regulator of human mast cells (MCs) and a potential mediator of allergy. In this study the effects of cyclosporin A (CSA) and FK-506, two potent immunosuppressive drugs, on SCF-dependent histamine release and growth of human MCs were analyzed. Preincubation of tissue MCs with CSA (3 micrograms/ml) resulted in inhibition of histamine release provoked by either recombinant human (rh) SCF (70.3% +/- 20.6% inhibition, p < 0.001) or anti-IgE (76.7% +/- 21.9%, p < 0.001) or by rhSCF+ anti-IgE (77.4% +/- 13.9%, p < 0.001). Almost the same inhibition was produced by FK-506 (rhSCF: 82.0% +/- 18.9% inhibition, p < 0.001; anti-IgE: 71.5% +/- 16.7%, p < 0.001; rhSCF+ anti-IgE: 70.0% +/- 7.3%, p < 0.001). The effects of CSA and FK-506 on SCF-dependent release of histamine were dose-dependent (IC50: CSA, 1 to 10 ng/ml; FK-506, 0.3 to 3 ng/ml). IC50 values about three to 10 times higher were found for MCs preincubated with rhSCF before anti-IgE activation, compared with anti-IgE or SCF alone. SCF-dependent differentiation of human MCs was analyzed in a long-term suspension culture system (n = 6). Unexpectedly, CSA and FK-506 were unable to suppress, but even enhanced SCF-dependent growth of MCs and formation of MC tryptase in long-term culture. Together, CSA and FK-506 inhibit SCF-dependent release of histamine from human MCs and even augment SCF-dependent growth of human MCs in long-term culture.

Cell Division↗
PubMed1996

Anti-IgE-induced accumulation of leukocytes, mediators, and albumin in skin chamber fluid from healthy and atopic subjects.

The aim of this study was to examine potential differences between healthy and atopic subjects with regard to IgE-mediated cutaneous inflammation. For this purpose, we analyzed histamine, tryptase, leukotriene B4, albumin, eosinophils, and total leukocytes in skin chamber fluid after challenge with anti-human IgE. We also measured gross skin reactivity (wheal, flare, and late-phase reactions), circulating IgE, and eosinophils, as well as the state of eosinophil activation. It was found that despite having more circulating IgE, the skin responsiveness of the atopic subjects did not differ significantly from that of the nonatopic subjects with respect to mediator release, albumin extravasation, or total recruitment of leukocytes. Moreover, the sizes of anti-IgE-induced wheal, flare, and late-phase reactions were very similar in the two groups. On the other hand, significant recruitment of eosinophils during the IgE-mediated reaction was more or less restricted to the atopic group. Yet the recruited eosinophils, of which the majority was in an early state of activation before degranulation, did not seem to contribute significantly to the IgE-mediated delayed skin edema. Furthermore, the eosinophil count in anti-IgE chambers of the atopic subjects did not correlate with any of the other parameters monitored. Thus because the anti-IgE-induced recruitment of eosinophils appeared to be unrelated to factors such as the number of peripheral blood eosinophils, the degree of mast cell activation, the intensity of inflammatory skin changes, and the level of circulating IgE, it is apparent that the mechanisms for and pathophysiologic role of IgE-mediated dermal eosinophil accumulation in atopic subjects require further investigation.

Antibodies, Anti-Idiotypic↗
PubMed1996

Mast cell effector mechanisms.

Several lines of evidence support the central role of the cysteinyl leukotrienes in aspirin-sensitive asthma, although their cellular source is unknown. The two most likely cells are the mast cell and eosinophil. Compared with aspirin-tolerant patients with asthma, patients with aspirin-sensitive asthma have been found to have a greater infiltration of mast cells and eosinophils in bronchial biopsy samples, although proportions of activated eosinophils were similar. Findings that support the involvement of mast cells include elevated serum histamine and tryptase levels after aspirin challenge in sensitive subjects, in line with a decrease in lung function and increased histamine and leukotriene C4 levels in nasal secretions; release of high-molecular-weight neutrophil chemotactic factor into serum after challenge; and prevention of aspirin-induced bronchoconstriction by pretreatment with cromolyn sodium or nedocromil sodium. These agents are also effective in protecting against bronchoconstriction induced by hyperosmolar stimuli, a challenge that is not associated with increased leukotriene E4 responsiveness but that is followed by increased release of histamine and prostaglandin D2 into bronchoalveolar lavage fluid. Antihistamines are poorly effective at inhibiting aspirin-induced bronchoconstriction but have been shown to attenuate the bronchoconstrictor response to hyperosmolar challenge. The main effector mechanism in hyperosmolar-induced bronchoconstriction appears to be mast cell activation and histamine release.

Animals↗
PubMed1997

Allergen binding to specific IgE in the nasal mucosa of allergic patients.

BACKGROUND: Until now, it has not been possible to identify specific IgE locally in the airway mucosa. In this study we investigated the possibility of determining specific allergen binding locally in the nasal mucosa. METHODS: Nasal mucosal biopsy specimens were taken from 11 patients with symptoms of an isolated grass pollen allergy, 10 patients with symptoms of perennial allergic rhinitis in response to house dust mite allergen, and 10 nonallergic control subjects. Sections of these biopsy specimens were stained by using commercially available biotinylated allergens (AlaSTAT, Diagnostic Products Corp.). RESULTS: Staining with biotinylated grass pollen (GP1) demonstrated positive cells only in patients with grass pollen allergy. Biotinylated Dermatophagoides pteronyssinus (D1) only stained cells in patients with perennial allergy. Specific binding of allergen to cells of patients with allergy and the blocking experiments proved the method to be highly specific. Allergen-positive cells stained double with IgE, the high-affinity receptor for IgE (Fc epsilon RI), CD1, HLA-DR, tryptase, and chymase. Most allergen-positive cells proved to be mast cells. CONCLUSION: This immunohistochemical study shows the presence of specific IgE against grass pollen and house dust mite allergens locally on cells in the airway mucosa.

Allergens↗
PubMed1997

Hymenoptera sting anaphylaxis and urticaria pigmentosa: clinical findings and results of venom immunotherapy in ten patients.

BACKGROUND: Occasional patients with urticaria pigmentosa and anaphylaxis after Hymenoptera stings have been described. In this situation the question arises: Is anaphylaxis IgE-mediated or induced by pharmacologic mediator release from mast cells? METHODS: We investigated 10 patients with histologically confirmed urticaria pigmentosa and a history of anaphylaxis after honeybee or Vespula stings before and during immunotherapy with the respective venom. RESULTS: In eight of 10 patients, an elevated serum tryptase level was found. In two of 10 patients, no venom-specific IgE could be detected by either skin tests or RAST. Five patients had no detectable venom-specific serum IgE, and in the remaining patients the level was low (<1 Phadebas RAST unit). Venom immunotherapy was well tolerated and caused only one mild systemic reaction in a patient during the dose increase phase. Six patients were re-stung while receiving venom immunotherapy: only one had a mild systemic reaction (angioedema) after a Vespula sting. CONCLUSION: Anaphylactic symptoms after Hymenoptera stings in patients with urticaria pigmentosa are most often IgE-mediated but can occasionally be observed in the absence of IgE sensitization to venom allergens. Venom immunotherapy can be safely and successfully used in patients with urticaria pigmentosa and sting anaphylaxis.

Adult↗