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Biomedical subjects

S R Durham

Publications and source records attributed to S R Durham.

At least 19 recordsLinked to original sources
PubMed1992

Cytokine messenger RNA expression for IL-3, IL-4, IL-5, and granulocyte/macrophage-colony-stimulating factor in the nasal mucosa after local allergen provocation: relationship to tissue eosinophilia.

Tissue eosinophilia is characteristic of human atopic allergic inflammation, although the mechanism is largely unknown. In this study we test the hypothesis that eosinophil infiltration during allergen-provoked rhinitis in hayfever sufferers may occur as a consequence of activation of a population of cells having a characteristic cytokine profile equivalent to the murine Th lymphocyte Th2 subset. Biopsies of the nasal inferior turbinate were obtained from 10 grass pollen-sensitive patients 24 h after local nasal provocation with allergen and after a control challenge with the allergen diluent. Biopsies were divided into two and subsequently processed for in situ hybridization using 35S-labeled RNA probes for selected cytokines and for immunohistology using an eosinophil granule mAb (EG2) which recognizes secreting eosinophils. At allergen-challenged sites compared with control sites there were significant increases in mRNA+ cells for IL-3 (p less than 0.04), IL-4 (p = 0.01), IL-5 (p = 0.02) and granulocyte/macrophage-CSF (p = 0.03). In contrast, only occasional hybridization signals were observed for IL-2 and IFN-gamma at both allergen and control sites. After allergen there was an increase (p = 0.01) in EG2+ eosinophils and significant correlations were observed between EG2+ cells and mRNA expression for "Th2-type" cytokines, particularly IL-5 (r = 0.90, p less than 0.0001). These results demonstrate that recruitment of eosinophils during human allergen-induced rhinitis is associated with cells expressing mRNA for IL-3, IL-4, IL-5, and granulocyte/macrophage-CSF.

Adult↗
PubMed1992

Preferential messenger RNA expression of Th1-type cells (IFN-gamma+, IL-2+) in classical delayed-type (tuberculin) hypersensitivity reactions in human skin.

We recently established that the allergen-induced late-phase cutaneous reaction in atopic subjects was associated with high mRNA expression for the cytokine gene cluster IL-3, IL-4, IL-5, and granulocyte/macrophage-CSF (GM-CSF), compared with IFN-gamma and IL-2, suggesting that allergic skin reactions contained the equivalent of murine Th2 cells. We now show that, in humans, classical delayed-type hypersensitivity is associated with cells preferentially expressing a Th1-type cytokine profile. Cryostat sections from skin biopsies from 24-h tuberculin reactions in 10 nonatopic subjects were hybridized with 35S-labeled RNA probes and processed by using in situ hybridization. On the whole, tuberculin biopsies showed preferential expression of mRNA encoding IFN-gamma and IL-2, although in some cases mRNA expression for IL-3, IL-4, IL-5, and GM-CSF was also observed. Biopsies from diluent control sites gave only occasional signals. The difference in the number of cells expressing mRNA in the diluent compared with tuberculin sites was statistically significant for IL-2 and IFN-gamma (p less than 0.01) but not for IL-3, IL-4, IL-5, and GM-CSF. These results suggest that cells infiltrating the site of the 24-h tuberculin reaction preferentially transcribe mRNA encoding IFN-gamma and IL-2, supporting the hypothesis that delayed-type hypersensitivity is associated with preferential activation of cells having a cytokine profile similar to the murine Th1 subset.

Adult↗
PubMed1992

Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma.

BACKGROUND: In atopic asthma, activated T helper lymphocytes are present in bronchial-biopsy specimens and bronchoalveolar-lavage (BAL) fluid, and their production of cytokines may be important in the pathogenesis of this disorder. Different patterns of cytokine release are characteristic of certain subgroups of T helper cells, termed TH1 and TH2, the former mediating delayed-type hypersensitivity and the latter mediating IgE synthesis and eosinophilia. The pattern of cytokine production in atopic asthma is unknown. METHODS: We assessed cells obtained by BAL in subjects with mild atopic asthma and in normal control subjects for the expression of messenger RNA (mRNA) for interleukin-2, 3, 4, and 5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon gamma by in situ hybridization with 32P-labeled complementary RNA. Localization of mRNA to BAL T cells was assessed by simultaneous in situ hybridization and immunofluorescence and by in situ hybridization after immunomagnetic enrichment or depletion of T cells. RESULTS: As compared with the control subjects, the subjects with asthma had more BAL cells per 1000 cell that were positive for mRNA for interleukin-2 (P less than 0.05), 3 (P less than 0.01), 4 (P less than 0.001), and 5 (P less than 0.001) and GM-CSF (P less than 0.001). There was no significant difference between the two groups in the number of cells expressing mRNA for interferon gamma. In the subjects with asthma, mRNA for interleukin-4 and 5 was expressed predominantly by T lymphocytes. CONCLUSIONS: Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.

Adult↗
PubMed1992

Activated T-lymphocytes and eosinophils in the bronchial mucosa in isocyanate-induced asthma.

We have studied the phenotype and activation status of leukocytes in the bronchial mucosa in patients with isocyanate-induced asthma. Fiberoptic bronchial biopsy specimens were obtained from nine subjects with occupational (five toluene- and four methylene diisocyanate-sensitive) asthma, 10 subjects with extrinsic asthma, and 12 nonatopic healthy control subjects. Bronchial biopsy specimens were examined by immunohistology with a panel of monoclonal antibodies and the alkaline phosphatase-antialkaline phosphatase method. There was a significant increase in the number of CD25+ cells (interleukin-2 receptor-bearing cells, presumed "activated" T-lymphocytes; p less than 0.01) in isocyanate-induced asthma compared with that of control subjects. There were also significant increases in major basic protein (BMK-13)-positive (p less than 0.02) and EG2-positive (p less than 0.01) cells that represent total and "activated" eosinophil cationic protein-secreting eosinophils, respectively. In agreement with our previous findings, CD25+ (p less than 0.01), BMK-13 (p less than 0.03), and EG2+ (p less than 0.01) cells were also elevated in extrinsic asthma. No significant differences were observed in the numbers of T-lymphocyte phenotypic markers (CD3, CD4, and CD8) between subjects with asthma (isocyanate-induced and extrinsic) and control subjects. Similarly, no significant differences in immunostaining for neutrophil elastase (neutrophils) or CD68 (macrophages) were observed. The results suggest that isocyanate-induced occupational asthma and atopic (extrinsic) asthma have a similar pattern of inflammatory cell infiltrate. The results support the view that T-lymphocyte activation and eosinophil recruitment may be important in asthma of diverse etiology.

Adult↗
PubMed1992

Immunohistology of the nasal mucosa in seasonal allergic rhinitis: increases in activated eosinophils and epithelial mast cells.

The immunohistology of the nasal mucosa was examined in 13 grass pollen-sensitive patients and in seven normal nonatopic control subjects before and during the pollen season. Cryostat sections (6 microns) of biopsy specimens from the inferior turbinate were immunostained with the alkaline-phosphatase antialkaline-phosphatase method and a panel of monoclonal antibodies. Mast cell subtypes were measured with a double sequential immunostaining method. Within the submucosa, seasonal increases in total (MBP+, p less than 0.01) and "activated" (EG2+, p less than 0.01) eosinophils were observed for the patients, which were significant when these counts were compared with counts for those of control subjects (MBP+ p less than 0.01; EG2+ p less than 0.001). Within the nasal epithelium, seasonal increases in total (p less than 0.05) and "activated" (p less than 0.02) eosinophils were also observed. Mast cell counts revealed seasonal increases in tryptase-only positive mast cell (MCT) (p less than 0.02) but not chymase plus tryptase-positive mast cells (MCTC) within the epithelium that were significant when counts were compared with those of control subjects (p less than 0.03). No significant changes were observed within the submucosa or epithelium for total leukocytes (CD45+ cells) or T-lymphocytes (CD3+, CD4+, CD8+, and CD 25+ cells) for either group. Similarly, no significant changes were observed for neutrophils (antielastase), macrophages (CD68+), nor HLA-DR+ cells. In the subjects with rhinitis, seasonal submucosal CD3+ counts correlated with MBP+ eosinophils (r = 0.56; p less than 0.05) and MCTS (r = 0.65; p less than 0.02). Similarly, seasonal epithelial EG2+ eosinophil counts correlated with MCTs (r = 0.56; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Asthma as an inflammatory disease: clinical perspectives.

Asthma is characterised by a persistent, ongoing airway submucosal inflammatory process which may underlie bronchial hyperresponsiveness and airways obstruction. Indirect assessment of airway inflammation includes examination of sputum or serum for eosinophils or eosinophil-derived products, but examination of bronchial mucosal biopsies or bronchoalveolar lavage fluid or cells remains the gold standard. Lymphocyte and eosinophil activation, with the release of certain cytokines such as interleukin-5, lipid mediators such as leukotrienes and eosinophil products such as major basic protein, may be important mechanisms of inflammation in asthma. Less invasive indirect measures of submucosal inflammation are needed to assess the impact of asthma treatment in the clinic. Antiinflammatory treatment in asthma should be introduced as early as possible. A greater understanding of the inflammatory mechanism or of the actions of corticosteroids may lead to the development of more effective and safer drugs for asthma.

Allergens↗
PubMed1992

Application of monoclonal antibodies against major basic protein (BMK-13) and eosinophil cationic protein (EG1 and EG2) for quantifying eosinophils in bronchial biopsies from atopic asthma.

A monoclonal antibody prepared against the eosinophil major basis protein (MBP) was compared with the anti-eosinophil cationic protein (ECP) antibodies (EG1 and EG2) in immunostaining of bronchial biopsies from atopic asthma and controls. Anti-MBP (designated BMK-13) did not cross-react with other eosinophil basic proteins (i.e. ECP, eosinophil peroxidase [EPO] or eosinophil-derived neurotoxin [EDN]) and stained more than 98% of peripheral blood eosinophils irrespective of their degree of activation. EG2 stained 15% of resting and 75% of activated eosinophils; EG1 recognized 74% and 78% of resting and activated cells, respectively. The numbers of BMK-13, EG1 or EG2-positive staining cells in bronchial biopsies from asthma were significantly greater than atopic non-asthmatics (P less than 0.02, P less than 0.01 and P less than 0.05, respectively) and normal non-atopic controls (P less than 0.001). For each of the various groups studied, the rank order for the number of eosinophils stained was BMK-13 greater than EG1 greater than EG2. BMK-13 stained significantly more cells from bronchial biopsies of atopic asthma and atopic non asthma when compared to EG2 (P less than 0.001 and P less than 0.05, respectively). Since only a proportion of BMK-13+ cells were EG2+, these results suggest that not all tissue eosinophils are actively secreting. Thus, BMK-13 can serve as a useful pan-eosinophil marker in tissue sections since it appears to stain most eosinophils.

Antibodies, Monoclonal↗
PubMed1992

Immunohistology of the nasal mucosa following allergen-induced rhinitis. Identification of activated T lymphocytes, eosinophils, and neutrophils.

We have studied the immunohistology of the nasal mucosa in allergen-induced rhinitis. Sixteen grass pollen-sensitive patients were challenged twice by randomly allocated allergen or control solutions applied on filter paper disks to the inferior turbinate. All had immediate nasal responses, but late-phase responses were equivocal and only evident as nostril blockage. When cell counts in the nasal submucosa were compared with control values 24 h after allergen, there were no changes in CD45+ (total leukocytes), CD3+, or CD8+ cells. Significant increases were found in the numbers of CD4+ T-helper cells (p less than 0.05) and CD25+ [interleukin-2 receptor (IL-2R+)] cells (p less than 0.02). Increases in eosinophils (anti-major basic protein, p less than 0.01) and neutrophils (antineutrophil elastase, p less than 0.01) were also observed. There were increases in tissue macrophages and HLA-DR-positive immunostaining and a reduction in mast cells (tryptase positive), but none of these changes was statistically significant. No significant changes in epithelial thickness, cross-sectional area, or integrity were observed. There was a significant correlation between CD4+ and CD25+ cells (r = 0.61, p less than 0.01) but not between macrophages and CD25+ cells (r = 0.18). The changes in the nasal submucosa were not merely a reflection of alterations in circulating cell populations since it was shown that a significant increase in the lymphocyte CD4/CD8 ratio (p less than 0.05) was observed in nasal biopsies but not in peripheral blood after allergen challenge.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Identification of T lymphocytes, macrophages, and activated eosinophils in the bronchial mucosa in intrinsic asthma. Relationship to symptoms and bronchial responsiveness.

Using immunohistochemistry and a panel of monoclonal antibodies, we have compared T-lymphocyte, eosinophil, macrophage, and neutrophil infiltration in bronchial biopsies from 10 intrinsic (nonallergic) asthmatics (IA) and seven extrinsic (allergic) asthmatic (EA), with similar degrees of disease severity. The results were compared with 12 normal healthy nonatopic controls (NC). All subjects were nonsmokers and were not taking oral or inhaled corticosteroids. An intense mononuclear cell infiltrate was identified in IA with an increase in the number of CD45+ cells (total leukocytes), CD3+ and CD4+ lymphocytes, and CD68+ macrophages (p < 0.03, p < 0.01, p < 0.03, and p < 0.03, respectively), compared with NC. Increases were also found in CD4+ (p < 0.05) and CD68+ (p < 0.05) cell numbers between IA and EA. IL-2 receptor-bearing cells (CD25+) and the number of total (MBP+) and actively secreting (EG2+) eosinophils, were also increased in IA compared with NC (p < 0.01, p < 0.01, and p < 0.01, respectively). Similar increases in EG2+ eosinophils and CD25+ (IL-2 receptor-positive) cells were observed in EA (p < 0.01 and p < 0.02, respectively). No differences were detected in the three groups for the number of elastase-positive cells (neutrophils). EG2+ numbers in IA correlated with the Aas asthma symptoms score (r = 0.65, p < 0.05), whereas EG2+ cell numbers in all asthmatics (IA + EA) correlated with airway methacholine responsiveness (r = -0.55, p < 0.03) and with the Aas asthma symptom score (r = 0.54, p < 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Co-expression of CD25 and CD3 in atopic allergy and asthma.

In an attempt to identify the phenotype of the CD25+ cells previously demonstrated in late-phase allergic reactions in skin and nasal mucosa, and in the bronchial mucosa in atopic asthma we have investigated the co-expression of CD3 and CD25 using double immunofluorescent staining. Fluorescein isothiocyanate (FITC) conjugated anti-CD3 monoclonal antibody and a biotinylated anti-CD25 monoclonal antibody (which was later developed with Texas Red streptavidin) were applied simultaneously to cryostat sections or cytospins of freshly prepared samples. Skin and nasal biopsies were from antigen-induced late-phase reactions, and bronchial biopsies and cytospins of bronchoalveolar lavage cells were from subjects with moderate atopic asthma. Four to 14% of CD3+ cells in these tissues were CD25+ and 61-100% of CD25+ cells also expressed CD3. However, CD25 was also expressed on non-CD3+ cells, assumed to be non-T cells. These results were comparable to that observed with a positive control of a tuberculin-challenged skin biopsy. Thus the majority of cells expressing CD25 in various types of atopic allergic inflammation in man were T lymphocytes.

Antigens, CD↗
PubMed1991

Messenger RNA expression of the cytokine gene cluster, interleukin 3 (IL-3), IL-4, IL-5, and granulocyte/macrophage colony-stimulating factor, in allergen-induced late-phase cutaneous reactions in atopic subjects.

Cryostat sections from skin biopsies from 24-h allergen-induced late-phase cutaneous reactions (LPR) in 14 human atopic subjects were hybridized with 35S-labeled RNA probes for a number of cytokines. mRNA was detected for interleukin 3 (IL-3) (8/14), IL-4 (10/14), IL-5 (11/14), and granulocyte/macrophage colony-stimulating factor (GM-CSF) (13/14). Only 5 of 14 gave hybridization signals for IL-2, and 0 of 14 for interferon gamma. Biopsies from diluent controls gave only occasional weak signals. These results suggest that cells infiltrating the site of the 24-h LPR transcribe mRNA for the IL-3, IL-4, IL-5, and GM-CSF gene cluster and support the hypothesis that atopy is associated with preferential activation of cells having a similar cytokine profile to the murine T helper type 2 subset.

Adolescent↗
PubMed1991

Usefulness of immunotherapy in patients with severe summer hay fever uncontrolled by antiallergic drugs.

OBJECTIVE: To evaluate the efficacy and safety of immunotherapy (hyposensitisation) in patients with severe summer hay fever. DESIGN: A randomised, double blind, placebo controlled study of a biologically standardised depot grass pollen extract. SETTING: Allergy clinic, Royal Brompton and National Heart Hospital, London. PATIENTS: 40 adults (mean age 35 years) with a history of severe grass pollen allergy uncontrolled by standard antiallergic drugs. Patients with perennial asthma were specifically excluded. INTERVENTION: Patients were randomised to receive either an active preparation (Alutard SQ, a grass pollen (Phleum pratense) extract) or placebo at a rate of two subcutaneous injections a week in increasing doses until a maintenance dose was reached. This maintenance dose was given once a month. MAIN OUTCOME MEASURES: Clinical efficacy was evaluated by symptom and drug diary cards, visual analogue scores during the grass pollen season, and a postseasonal assessment by the patients and a doctor. Conjunctival and skin sensitivity to local allergen provocation was measured before and after eight months of treatment. RESULTS: There was a highly significant decrease (median Alutard SQ v median placebo (95% confidence interval for difference between medians] in total symptom scores (p=0.001) in the Alutard SQ treated group (360 v 928 (238 to 825]. Significant differences were also found in total drug use (p=0.002, 129 v 627 (178 to 574]. Visual analogue symptom scores were also reduced in the active group (p=0.02, 2.2 v 5.5 (-4.8 to -0.5]. The postseasonal assessment, by either the doctor or the patients, showed a large improvement (p less than 0.001) in favour of Alutard SQ. Provocation tests showed a greater than 10-fold reduction for the active group in immediate conjunctival allergen sensitivity (p=0.001), a 40% decrease in early phase response (p=0.02), and a 57% decrease in the late phase (p=0.001) cutaneous response after intradermal allergen. A total of 523 active injections were given. There was one systemic reaction at 10 minutes after injection, which was rapidly reversed with intramuscular adrenaline. There was one mild delayed urticarial reaction at 2 1/2 hours. CONCLUSION: Immunotherapy is effective in patients with severe summer hay fever, but immediate anaphylactic reactions limit its use to specialised centres. Patient selection is extremely important, and chronic perennial asthma should be specifically excluded. As serious reactions occur within minutes a two hour wait for all patients after each injection seems unnecessary.

Adult↗
PubMed1991

Eosinophils, T-lymphocytes, mast cells, neutrophils, and macrophages in bronchial biopsy specimens from atopic subjects with asthma: comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness.

Bronchial biopsy specimens were obtained by fiberoptic bronchoscopy from 21 atopic subjects with asthma, 10 atopic subjects without asthma, and 12 normal healthy control subjects. With immunohistochemical techniques and a panel of monoclonal antibodies, inflammatory cells were identified and counted in the bronchial mucosa. The mean number of leukocytes (CD45+) and T-lymphocytes (CD3+, CD4+, and CD8+) at two airway levels in the subjects with asthma tended to be higher than in the other groups, but this difference did not achieve statistical significance. Similarly, there were no significant differences in the numbers of mucosal-type or connective tissue-type mast cells, elastase-positive neutrophils, or Leu-M3+ cells in the airway mucosa of subjects with asthma compared with atopic subjects without asthma and healthy control subjects. In contrast, significantly more interleukin-2 receptor-positive (CD25+) cells and "activated" (EG2+) eosinophils (EOSs) were present in the airways of subjects with asthma at both proximal and subsegmental biopsy sites. When the relationships between numbers of T-lymphocytes, activated (CD25+) cells, and EOSs were analyzed, there were positive correlations between CD3 and EG2, between CD3 and CD25, and between CD25 and EG2 positive cells in the airways of subjects with asthma. Furthermore, the ratio of EG2+ to CD45+ cells correlated with the provocative concentration of methacholine that caused a 20% decrease of FEV1 in hyperresponsive subjects. Although these associations do not prove a causal relationship, the results support the hypothesis that activated (CD25) T-lymphocytes release products which regulate recruitment of EOSs into the airway wall. In addition, our findings suggest that, in the large airways at least, asthma is not associated with hyperplasia of either mucosal-type or connective tissue-type mast cell.

Adult↗
PubMed1991

CBF measured by Xe-CT: approach to analysis and normal values.

Normal reference values and a practical approach to CBF analysis are needed for routine clinical analysis and interpretation of xenon-enhanced computed tomography (CT) CBF studies. We measured CBF in 67 normal individuals with the GE 9800 CT scanner adapted for CBF imaging with stable Xe. CBF values for vascular territories were systematically analyzed using the clustering of contiguous 2-cm circular regions of interest (ROIs) placed within the cortical mantle and basal ganglia. Mixed cortical flows averaged 51 +/- 10ml.100g-1.min-1. High and low flow compartments, sampled by placing 5-mm circular ROIs in regions containing the highest and lowest flow values in each hemisphere, averaged 84 +/- 14 and 20 +/- 5 ml.100 g-1.min-1, respectively. Mixed cortical flow values as well as values within the high flow compartment demonstrated significant decline with age; however, there were no significant age-related changes in the low flow compartment. The clustering of systematically placed cortical and subcortical ROIs has provided a normative data base for Xe-CT CBF and a flexible and uncomplicated method for the analysis of CBF maps generated by Xe-enhanced CT.

Adult↗
PubMed1991

The significance of late responses in asthma.

There is good evidence to suggest that the late response is a valid clinical model of asthma. The factors which predict late responses in individual subjects are unknown although recent studies suggest that the level of IgE sensitivity and allergen dose are two important variables. Recent placebo-controlled pharmacological studies support earlier work and vindicate the use of late responses as a preclinical screening test in the evaluation of new therapeutic agents. In addition to putative pro-inflammatory mechanisms we should evaluate possible protective mechanisms which might prevent the development of late responses in individual subjects. In this regard, altered adrenal responses as reflected by serum cortisol concentrations did not appear to play a role, protective or otherwise in the development of late asthmatic responses. In conclusion, the development of symptomatic late responses and associated increased bronchial responsiveness are relevant to day-to-day asthma. As suggested by Cockcroft, repeated allergen exposure may result in a vicious cycle of ongoing bronchial inflammation. This emphasizes the importance of allergen avoidance and the need for earlier intervention in mild to moderate asthma with effective prophylactic agents which are known to inhibit late responses.

Asthma↗
PubMed1991

Immunotherapy and allergic inflammation.

A double-blind placebo-controlled trial of allergen injection immunotherapy in adult patients with severe summer hayfever. We used a partially purified biologically standardised grass pollen depot preparation (Alutard SQ, ALK Denmark Ltd.). Immunotherapy was extremely effective in reducing symptoms and medication requirements. Clinical improvement was accompanied by a decrease in both a target organ (conjunctival) and skin sensitivity. The injections were well-tolerated with minimal side effects. The results suggest that 30 minutes rather than 2 hours is an acceptable post-injection observation period. Successful immunotherapy was accompanied by suppression of the late cutaneous response to allergen. Specific immunostaining of skin biopsies revealed inhibition of the characteristic CD4+ T cell and EG2+ activated eosinophil cellular infiltrate during the late response. There was a significant relationship between CD4+ T cell and eosinophil counts after immunotherapy, i.e. the lower the number of infiltrating CD4+ cells, the lower the eosinophil counts. An unexpected finding was a prominent CD25+ (interleukin-2 receptor positive) cellular infiltrate which was only observed following Alutard SQ. Further studies involving double immunostaining methods should identify the phenotype of these activated, IL-2R+ cells. Based on murine studies Mosmann and colleagues have classified T cell responses into two types according to their profile of lymphokine production [11]. TH1 cells produce predominantly the IL-4 family of cytokines (IL-3, IL-4, IL-5) whereas TH2 cells produce predominantly interleukin-2 and interferon gamma. Insofar as the Mosmann classification may possibly be relevant to human T cell responses, the above findings would support a switch from a "TH2-" to a "TH1-" lymphocyte response following immunotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

TNF alpha mRNA expression in allergic inflammation.

Using the technique of in situ hybridization, we have attempted to identify messenger RNA for tumour necrosis factor-alpha (TNF alpha) in cells infiltrating allergen-induced late phase reaction (LPR) of the skin and the nose of atopic subjects. We have also compared the number of TNF alpha mRNA positive cells in bronchoalveolar lavage (BAL) from atopic asthmatics and normal controls. Twenty-four hours after local allergen challenge, 12/14 skin biopsies and 9/10 nasal biopsies had positive hybridization signals for TNF alpha mRNA whereas only 4/14 and 2/10 biopsies were positive in the relevant diluent controls. Compared with diluent sites significantly increased numbers of cells expressing mRNA for TNF alpha were observed in the LPR of skin (P less than 0.004) and nose (P less than 0.006). All BAL from asthmatics (n = 10) and from normal volunteers (n = 10) had cells showing positive hybridization signals for TNF alpha mRNA but these were at increased frequency in asthmatics (P less than 0.001). These results suggest that TNF alpha may be an important cytokine in atopic allergic inflammation.

Adolescent↗