Search PubMed⌕ Search

Biomedical subjects

S R Durham

Publications and source records attributed to S R Durham.

At least 91 records · Page 5Linked to original sources
PubMed1997

Nasal nitric oxide is increased in patients with asthma and allergic rhinitis and may be modulated by nasal glucocorticoids.

Nitric oxide (NO) is produced in large amounts in the noses of normal individuals. We have measured NO by chemiluminescence in the noses and exhaled air of subjects with symptomatic allergic rhinitis, some of whom had concomitant asthma, during the pollen season and compared this with values measured in normal subjects and in patients treated with nasal and/or inhaled glucocorticoids. We found that nasal levels of NO were significantly (p < 0.001) elevated in patients with untreated rhinitis (1527 +/- 87 ppb, n = 12) compared with normal individuals (996 +/- 39 ppb, n = 46) or subjects treated with nasal steroids (681 +/- 34 ppb, n = 10), whereas exhaled NO in patients with untreated rhinitis was similar to that in normal subjects (10 +/- 2 ppb vs 7 +/- 0.6 ppb, respectively). In five subjects who were nasally challenged with allergen, there was a significant decrease in nasal NO 1 hour after challenge, and this was significantly correlated with increased rhinitis symptoms. In patients with rhinitis and concomitant asthma, nasal NO was also significantly elevated (1441 +/- 76 ppb, n = 16) but not when they were treated with nasal or inhaled steroids; whereas exhaled NO was elevated in untreated patients and in patients treated with nasal, but not inhaled, steroids. Our data suggest that the increase in exhaled NO in patients with allergic rhinitis is likely to be due to increased local production, caused by long-term exposure to allergen, which is suppressed by locally administered steroids. Measurement of nasal NO may be useful to study the inflammatory response in rhinitis and its response to antiinflammatory treatments.

Administration, Inhalation↗
PubMed1997

Skin prick testing in general practice: a pilot study.

Allergy skin prick testing is regarded as a routine diagnostic procedure in hospital settings, but its role in general practice is not yet defined. Our aim was to explore the ways in which skin prick testing might facilitate the work of general practice nurses engaged in asthma patient care. A structured questionnaire was completed by 18 practice nurses before and again after administering allergy skin tests to four common aeroallergens (dust mite, grass pollen, cat and dog danders) to 319 consecutive attenders with known or suspected asthma. Nurses' decisions about whether or not to give allergen avoidance advice were reversed after skin testing in 63 (22%) cases for dust mite, 67 (23%) cases for grass pollen, 38 (13%) cases for cat fur and 49 (17%) cases for dog hair. Had allergen avoidance interventions been targeted only at patients with both a positive skin test and a positive clinical history, the number of planned interventions would have declined from 305 before skin testing to 142 after. The findings suggest that allergy skin prick testing was feasible and acceptable in general practice, and that one role may be to reduce the number of allergen avoidance interventions offered to patients unlikely to benefit.

Adolescent↗
PubMed1997

Effect of cyclosporin A on the allergen-induced late asthmatic reaction.

BACKGROUND: The allergen-induced late asthmatic reaction (LAR) is associated with mucosal inflammation involving several cell types including activated T lymphocytes and eosinophils. In contrast, the early asthmatic reaction (EAR) is considered to results from rapid allergen-induced release of bronchoconstrictor mediators from IgE sensitised mast cells. Cyclosporin A has efficacy in chronic severe corticosteroid-dependent asthma and is believed to act principally by inhibiting cytokine mRNA transcription in T lymphocytes. However, it has effects on other cell types in vitro, including the inhibition of exocytosis/degranulation events in mast cells. It was therefore hypothesised that cyclosporin A would attenuate both the EAR and LAR in subjects with mild asthma. METHODS: Twelve sensitised atopic asthmatic subjects with documented dual asthmatic responses were studied in a double blind, placebo controlled, crossover trial. On two separate study visits subjects received two oral doses of either cyclosporin A or matched placebo before inhaled allergen challenges. The forced expiratory volume in one second (FEV1) was measured half hourly for eight hours and blood eosinophil counts were analysed three, six, and 24 hours after the challenge. Treatment effects on blood eosinophil counts as well as the EAR and LAR, respectively defined as the areas under the curve (AUC) of FEV1 changes from baseline between 0-1 and 4-8 hours after challenge, were compared by non-parametric crossover analysis. RESULTS: Cyclosporin A reduced both the LAR (median AUC -41.9 1.h (interquartile range -82.7 to -12.4) for cyclosporin A and -84.5 1.h (-248.9 to -39.1) for placebo; p = 0.007) and the late increase in blood eosinophils (median 0.2 x 10(9)/1 (0.15 to 0.4) for cyclosporin A and 0.4 x 10(9)/1 (0.25 to 0.55) for placebo; p = 0.024) but had no effect on the EAR. The reduction of the LAR by cyclosporin A correlated significantly with prechallenge blood concentrations of cyclosporin A (r = 0.6, p = 0.028). CONCLUSIONS: These data are consistent with the concept that cyclosporin A has anti-inflammatory actions in asthma resulting from inhibition of mRNA transcription of eosinophil-active cytokines, predominantly in T lymphocytes. Cyclosporin A, possibly in its inhaled form, or other agents which prevent cytokine gene transcription may therefore have potential in ameliorating the inflammatory component of asthma.

Adult↗
PubMed1997

RANTES in human allergen-induced rhinitis: cellular source and relation to tissue eosinophilia.

Human allergen-induced rhinitis is associated with recruitment and activation of CD4+ T lymphocytes and eosinophils. RANTES is a novel CC chemokine that is a potent chemoattractant for both memory T cells and eosinophils. We therefore investigated RANTES in the nasal mucosa after local allergen provocation. Nasal lavage was performed, and biopsies from the inferior nasal turbinate were taken from 14 atopic, seasonal rhinitic patients and seven normal subjects for as long as 6 h after challenge with a grass pollen extract and after a control (allergen diluent) challenge. In five of seven rhinitics tested, radioimmunoassay of nasal fluid demonstrated increases in RANTES at 2 to 4 h (p < 0.05). Nasal allergen challenge provoked significant increases in RANTES mRNA (p = 0.0015) and protein (p = 0.01) containing cells in the nasal submucosa at 6 h. No changes were observed in normal subjects. Increases in RANTES mRNA+ cells correlated with the associated increases in eosinophils (r = 0.78, p = 0.001). Colocalization studies revealed that the majority of RANTES mRNA+ cells were macrophages (51%) followed by eosinophils (15%), T lymphocytes (11%), and mast cells (3%). Our results demonstrate that allergen-induced rhinitis is associated with release of RANTES and upregulation of RANTES mRNA and protein+ cells, predominantly macrophages, in the nasal mucosa. RANTES synthesis, release, or receptor antagonism may represent a potential target for antiallergy treatment.

Adult↗
PubMed1997

Membrane-bound and soluble alpha IL-5 receptor mRNA in the bronchial mucosa of atopic and nonatopic asthmatics.

Eosinophilic inflammation and interleukin-5 (IL-5) expression are characteristic features of the bronchial mucosa in asthma. We have investigated the differential expression of membrane and soluble isoforms of alpha IL-5 receptor (alpha IL-5Rm and alpha IL-5Rs) mRNA in asthmatics and in normal control subjects and examined the correlation between alpha IL-5Rm and alpha IL-5Rs expression and the FEV1 and airway hyperresponsiveness. Nineteen subjects with stable asthma (atopic = 9; intrinsic = 10) and 22 control subjects (atopic = 12; nonatopic = 10) were recruited. Endobronchial biopsies were obtained and processed for in situ hybridization and double-staining techniques. There was a significant increase in the number of cells per millimeter basement membrane expressing mRNA for total, membrane-bound, and soluble alpha IL-5R in asthmatics when compared with that in nonasthmatic control subjects (p < 0.001); 93% of the cells positive for alpha IL-5R mRNA were EG2+ve eosinophils. There was no significant difference in the expression of alpha IL-5Rm and alpha IL-5Rs between the atopic and nonatopic asthmatics. The expression of alpha IL-5Rm and alpha IL-5Rs was also nonsignificantly different between the atopic and nonatopic control subjects. However, in the asthmatic subjects, the number of positive cells expressing mRNA for alpha IL-5Rm inversely correlated with FEV1(r2 = 0.89, p < 0.001), whereas the expression of alpha IL-5Rs mRNA directly correlated with FEV1 (r2 = 0.52, p < 0.001). There were no significant correlations between alpha IL-5R isoforms and the methacholine PC20. These results suggest that alpha IL-5R upregulation and differential regulation of alternatively spliced alpha IL-5R mRNA transcripts may influence the eosinophil response and the accompanying changes in airflow limitation in both atopic and nonatopic variants of chronic asthma.

Adult↗
PubMed1997

Relationship between IL-4 and IL-5 mRNA expression and disease severity in atopic asthma.

Atopic asthma is characterized by chronic inflammation of the bronchial mucosa in which eosinophil- and immunoglobulin E (IgE)-dependent mechanisms are believed to be prominent. Therefore, specific proeosinophilic mediators such as interleukin (IL)-5 and essential cofactors for IgE switching in B-lymphocytes such as IL-4 could play a pivotal role in asthma. However, the exact role that individual inflammatory mediators play in the development of the disease in humans is still unknown. Using semiquantitative reverse transcriptase-polymerase chain reaction amplification in bronchial biopsies from 10 atopic asthmatics, we have tested the hypothesis that IL-4 and IL-5 mRNA expression relative to beta-actin mRNA correlates with validated indicators of disease severity. IL-4 and IL-5 mRNA copies relative to beta-actin mRNA were detected in bronchial biopsies from atopic asthmatics. The numbers of IL-5 mRNA copies relative to beta-actin mRNA correlated with disease severity assessed by the Aas asthma score (r = 0.70, p = 0.01), baseline FEV1 (r = -0.94, p = 0.001), baseline peak expiratory flow rate (r = -0.77, p = 0.01), peak expiratory flow rate variability over 2 wk (r = 0.69, p = 0.028), and the histamine PC20 (r = -0.72, p = 0.018). Conversely, the numbers of IL-4 mRNA copies relative to beta-actin mRNA did not correlate with asthma severity, but they positively correlated with total serum IgE concentrations (r = -0.90, p = 0.001). Our present results support the concept that IL-5 may determine asthma clinical expression and severity, and by inference they support the development of IL-5 targeted therapies.

Asthma↗
PubMed1997

Bronchial mucosal expression of the genes encoding chemokines RANTES and MCP-3 in symptomatic atopic and nonatopic asthmatics: relationship to the eosinophil-active cytokines interleukin (IL)-5, granulocyte macrophage-colony-stimulating factor, and IL-3.

Intrinsic (nonatopic) asthma is considered to be a distinct pathogenetic variant of asthma since, unlike extrinsic (atopic) asthma, patients are skin-prick test negative to common aeroallergens and have total serum immunoglobulin E concentrations within the normal range. However both atopic and nonatopic asthma are characterized by chronic inflammation of the bronchial mucosa in which eosinophils are prominent and are believed to be associated with local tissue damage. Therefore, specific eosinophil chemoattractants acting in concert with factors which prolong eosinophil survival may at least partly account for selective eosinophil recruitment to the asthmatic bronchial mucosa. The CC chemokines RANTES and monocyte chemotactic protein 3 (MCP-3) are potent eosinophil chemotactic factors, while the cytokines interleukin (IL)-5, granulocyte macrophage-colony-stimulating factor (GM-CSF), and IL-3 prolong eosinophil survival. We have tested the hypothesis that elevated numbers of cells expressing mRNA for RANTES and MCP-3, as well as IL-5, GM-CSF, and IL-3 are present in bronchial biopsies from atopic and nonatopic asthmatics compared with atopic and nonatopic nonasthmatic controls. The technique of in situ hybridization using 35S-labeled riboprobes was employed to detect mRNA+ bronchial mucosal cells. Compared with controls we observed significant increases in the numbers of cells expressing RANTES and MCP-3, as well as IL-5, GM-CSF, and IL-3 (all P values < 0.001) in atopic and nonatopic asthmatics. These observations support the view that atopic and nonatopic asthma are associated with combined bronchial mucosal expression of CC chemokines (RANTES and MCP-3), together with eosinophil-active cytokines (IL-5, GM-CSF, and IL-3). These cytokines might contribute to the bronchial mucosal accumulation of activated eosinophils in both atopic and nonatopic variants of asthma.

Asthma↗
PubMed1997

IL-13 mRNA and immunoreactivity in allergen-induced rhinitis: comparison with IL-4 expression and modulation by topical glucocorticoid therapy.

The allergen-induced late nasal response (LNR) is associated with high expression of interleukin-4 (IL-4) and IL-5 messenger RNA (mRNA) in the nasal mucosa, suggesting a role for Th2-type cytokines in the development of the LNR. Moreover, topical corticosteroid-mediated inhibition of the LNR is accompanied by inhibition of IL-4, but not IL-5, mRNA expression, IL-13 shares a number of functions with IL-4, including IgE switching and vascular cell adhesion molecule-1 (VCAM-1) upregulation. We investigated the expression of IL-13 mRNA and immunoreactivity in nasal biopsies from 10 normal subjects and 20 subjects with allergic rhinitis. IL-4 mRNA expression was examined in the same subjects. The allergic rhinitis patients were randomized to receive a 6-wk treatment with either topical fluticasone propionate (n = 10) or placebo (n = 10) nasal spray twice daily. A nasal biopsy was taken before treatment and 24 h after local nasal allergen provocation with a grass-pollen extract. Before treatment, there was no significant difference between the allergic rhinitis patients and controls in the expression of IL-13 mRNA and immunoreactivity. After allergen provocation, we observed a significant increase in IL-13 mRNA-positive and immunoreactive cells at 24 h only in subjects given placebo (P < 0.001). Inhibition of the LNR after corticosteroid treatment was associated with a marked decrease in allergen-induced IL-13 mRNA-positive (P < 0.001) and immunoreactive cells (P < 0.001). In subjects given placebo, 76.9 +/- 5.5% of IL-13 mRNA-positive cells observed after allergen were CD3+, whereas 11.2 +/- 2.7% coexpressed immunoreactivity for mast-cell tryptase. In these subjects, increases in cells expressing IL-13 mRNA were greater than for IL-4 mRNA (P = 0.001), and double in situ hybridization studies revealed that 100% of the IL-4 mRNA-positive cells coexpressed IL-13 mRNA, whereas 66.6 +/- 10.5% of IL-13 mRNA-positive cells coexpressed IL-4 transcripts after allergen challenge. The results of this study suggest that IL-13 expression is a prominent feature of the LNR, and that inhibition of the LNR following steroid therapy may be partly attributable to inhibition of IL-13 expression.

Administration, Intranasal↗
PubMed1996

Human eosinophils express messenger RNA encoding RANTES and store and release biologically active RANTES protein.

Eosinophils synthesize and store various cytokines with potential autocrine activity. We hypothesized that eosinophils synthesize and store RANTES, a CC-chemokine with potent eosinophil chemotactic activity. Expression of RANTES mRNA in highly purified eosinophil populations was detected by reverse transcription followed by polymerase chain reaction analysis. In situ hybridization (ISH) with 35S-labeled RANTES-specific riboprobes showed that 6.8-10% of peripheral blood eosinophils obtained from atopic subjects expressed RANTES mRNA, increasing to 25% after incubation (16 h) with interferon (IFN)-gamma, but not ionomycin in vitro. Peripheral blood eosinophils also showed specific immunoreactivity with an anti-RANTES monoclonal antibody, consistent with translation of the mRNA. By enzyme-linked immunosorbent assay, blood eosinophils were shown to contain a median of 7300 pg (range 5200-8800) RANTES per 10(6) cells, of which a mean of 24% was released into culture supernatants after stimulation of the cells with serum-coated particles in vitro. These culture supernatants exhibited eosinophil chemotactic activity which was inhibited (mean 68%) by a specific anti-RANTES antibody. Sequential immunocytochemistry and ISH on biopsies obtained from allergen-induced late-phase cutaneous reactions showed that 55-75% of the infiltrating RANTES mRNA+ cells were EG2+ eosinophils. Allergen, but not diluent challenge, was also associated with a time-dependent increase in the number of cells showing RANTES immunoreactivity. Of these cells, 55% were identified as eosinophils by morphological criteria. Thus, human eosinophils have the capacity to synthesize, store and secrete physiologically relevant quantities of RANTES, and may therefore be an important source of this chemokine in allergic inflammation.

Allergens↗
PubMed1996

Grass pollen immunotherapy inhibits allergen-induced infiltration of CD4+ T lymphocytes and eosinophils in the nasal mucosa and increases the number of cells expressing messenger RNA for interferon-gamma.

BACKGROUND: Grass pollen injection immunotherapy is effective in patients with summer hay fever, although efficacy must be balanced against possible side effects. The mechanism of immunotherapy is unknown but may be related to its ability to inhibit allergen-induced late responses, which are known to be characterized by infiltration of T lymphocytes, eosinophils, and cells with messenger RNA for so-called TH2-type cytokines (IL-4 and IL-5). OBJECTIVE: This study was designed to observe the effect of grass pollen immunotherapy on late nasal responses and associated cellular infiltration and cytokine mRNA expression. METHODS: We performed local nasal provocation with grass pollen (and a control challenge) in 28 patients after a 12-month double-blind, placebo-controlled trial of immunotherapy. Nasal biopsy specimens were obtained at 24 hours and processed for immunohistology and in situ hybridization studies. RESULTS: Grass pollen immunotherapy inhibited allergen-induced immediate (0 to 60 minutes) increases in sneezing (p < 0.02) and nasal blocking (p < 0.01) and late (0 to 24 hours) nasal symptoms (p < 0.05). Immunotherapy also inhibited the associated infiltration of the nasal mucosa by CD4+ T lymphocytes and total (major basic protein-containing) and "activated" (cationic protein-secreting) eosinophils (all p = 0.03). There was a significant (p = 0.04) increase in cells expressing mRNA for interferon-gamma at 24 hours after allergen challenge, which correlated inversely with patients' seasonal symptoms (r = -0.65, p < 0.05) and medication requirements (r = -0.75, p < 0.02) during the pollen season. CONCLUSION: The results suggest that successful grass pollen immunotherapy for summer hay fever may act by inhibiting allergen-induced T lymphocyte and eosinophil recruitment and eosinophil activation in the target organ, possibly through a mechanism involving protective local increases in TH1-type cells.

Adult↗
PubMed1996

Effect of cetirizine and prednisolone on cellular infiltration and cytokine mRNA expression during allergen-induced late cutaneous responses.

BACKGROUND: The ability of cetirizine to inhibit eosinophil infiltration into the sites of allergen-induced cutaneous late-phase reactions is controversial. A previous skin biopsy study gave negative results with 15 mg of cetirizine as a single dose. OBJECTIVE: To confirm these findings we have used cetirizine (30 mg daily) for 5 days and compared the results with prednisolone (20 mg daily for 5 days) as a positive control. The effect of these agents on mRNA positive cells for interleukin-3 (IL-3), interleukin-4, interleukin-5 and granulocyte/macrophage-colony stimulating factor (GM-CSF) was also evaluated. METHODS: A double-blind, placebo-controlled cross-over study (n = 12) was followed. After each treatment 30 biological units (BUs) of Dermatophagoides pteronyssinus or Phleum pratense were injected intradermally and the early (15 min) and late-phase response sizes (6 and 24 h) were measured. Skin biopsies were taken at 24 h for immunocytochemistry and in situ hybridization. RESULTS: Cetirizine but not prednisolone inhibited the early-phase response (37%, P = 0.004). In contrast prednisolone, but not cetirizine, significantly inhibited the size of the late-phase reaction at 24 h (70%, P = 0.021). This was associated with significant decreases in total (MBP+) and activated (EG2+) eosinophils (P = 0.019 and 0.014, respectively), as compared with placebo. There were also clear but non-significant reductions in interleukin-3, interleukin-4, interleukin-5 and granulocyte/macrophage-colony stimulating factor mRNA+ cells. CONCLUSION: Prednisolone, but not cetirizine, inhibited both the magnitude of the allergen-induced late-phase response and the accompanying local eosinophil infiltration. These corticosteroid effects were associated with a reduction in cells expressing mRNA for 'TH2-type' cytokines.

Adult↗
PubMed1996

Safety of fibreoptic bronchoscopy in asthmatic and control subjects and effect on asthma control over two weeks.

BACKGROUND: Concerns remain about the safety of bronchoscopy in asthma and there are few data on the effect of this procedure on asthma control in the days or weeks following bronchoscopy. METHODS: In an initial study of bronchoalveolar lavage and bronchial biopsies in asthmatic and control subjects, data on peak expiratory flow rates (PEFR) collected prospectively before and after the procedure were available from 21 of the 29 asthmatic subjects studied. These showed a median 23% fall in PEFR from baseline after bronchoscopy (range 3-58%). To determine whether this fall in PEFR following bronchoscopy reflected bronchospasm or the effect of sedation, PEFR and spirometric tests were performed during the two hours following bronchoscopy in a further study of 15 symptomatic asthmatic subjects and 20 non-asthmatic controls. To examine the effect on asthma control, asthmatic patients recorded PEFR, symptom scores, and medication use for two weeks before and after bronchoscopy. RESULTS: After bronchoscopy with bronchial biopsies there was no difference between the median maximal fall in either PEFR or arterial oxygen saturation between the 15 asthmatic patients (10.4% and 4%, respectively) and 20 controls (12% and 3%). Moreover, there were no significant changes in PEFR, symptom score, or medication use by the asthmatic subjects in the two weeks after bronchoscopy when compared with the two weeks before bronchoscopy. CONCLUSIONS: Fibreoptic bronchoscopy is well tolerated in asthmatic subjects. Falls in PEFR in both asthmatic and non-asthmatic subjects after bronchial biopsy may reflect the effects of sedation rather than bronchospasm. Additional bronchoalveolar lavage may cause bronchoconstriction. Careful monitoring is therefore essential. Peak flow monitoring up to two weeks after bronchoscopy with bronchial biopsy revealed no delayed effects on asthma control.

Adolescent↗
PubMed1996

Prednisolone treatment in asthma. Reduction in the numbers of eosinophils, T cells, tryptase-only positive mast cells, and modulation of IL-4, IL-5, and interferon-gamma cytokine gene expression within the bronchial mucosa.

We have tested the hypothesis that the beneficial effects of corticosteroids in asthma may result from reduction in the number of inflammatory cells infiltrating the bronchial mucosa with inhibition of cytokine gene expression. A randomized parallel group study was performed in 18 moderately severe asthmatic patients in whom an elective trial of corticosteroid treatment was indicated. Fiberoptic bronchoscopy was performed and bronchial biopsies taken from segmental carinae before and after 2 wk treatment with prednisolone (0.6 mg/kg/d) or matched placebo tablets. Immunohistology was performed on 6-microns cryostat sections using monoclonal antibodies. The number of cells expressing cytokine messenger RNA (mRNA) was assessed by in situ hybridization using S35-labeled riboprobes. When prednisolone- and placebo-treated groups were compared there was a decrease in airway methacholine responsiveness (p < 0.01) and an increase in FEV1 (p < 0.05) after prednisolone. This was accompanied by a reduction in CD3+ T lymphocytes (p < 0.05), "activated" EG2+ eosinophils (p < 0.02), and tryptase-only (mucosal-type) MCT cells (p < 0.02) but not MCTC (tryptase+chymase positive) cells in prednisolone-treated patients. In prednisolone-treated patients there was also a reduction in the number of cells expressing mRNA for interleukin-4 (IL-4, p < 0.01), and interleukin-5 (IL-5, p < 0.03) and an increase in cells expressing mRNA for interferon-gamma (IFN-gamma) (p < 0.01). These results support the view that corticosteroid treatment in asthma may act by modulation of cytokine expression with consequent inhibition of the local bronchial inflammatory infiltrate and tissue eosinophilia.

Adult↗
PubMed1996

High-affinity IgE receptor (FcepsilonRI)-bearing cells in bronchial biopsies from atopic and nonatopic asthma.

Asthma is characterized by bronchial mucosal inflammation. Although allergen-induced activation of cells binding allergen-specific immunoglobulin E (IgE) through high-affinity receptors (Fc(epsilon)RI) is believed to play some role in asthma, inappropriate synthesis of total or allergen-specific IgE cannot be demonstrated in some ("intrinsic") patients despite the fact that the nature of the bronchial inflammation is similar to that in atopic ("extrinsic") asthmatics. We have studied the numbers and phenotype of Fc(epsilon)RI-bearing cells in bronchial biopsies from 12 atopic and 10 nonatopic asthmatic patients and compared our findings with 10 atopic and 12 nonatopic control subjects using single and double immunohistochemistry. Significantly increased numbers of Fc(epsilon)RI-bearing cells were identified in bronchial biopsies from atopic and nonatopic asthmatics and atopic control subjects when compared with normal controls (p = 0.001, 0.006, and 0.0006, respectively). In asthmatics and atopics the majority of Fc(epsilon)RI-bearing cells were identified as mast cells and macrophages; a much smaller percentage were eosinophils. We conclude that elevated numbers of high-affinity IgE receptor-bearing cells are a feature of bronchial biopsies of asthmatic subjects, irrespective of their atopic status.

Adult↗