ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01102.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01103.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01104.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01105.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01106.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SummaryBackgroundSkin tests and tests for IgE antibodies show that subjects are usually sensitive to a number of different pollens, frequently from taxonomically diverse species which are assumed to be allergenically non‐crossreactive. This suggests that the presence of IgE antibody‐reactivity to an individual pollen may not necessarily have resulted from contact with that pollen or even with a taxonomically closely related species.ObjectiveSince this has important consequences for allergen avoidance and desensitization of patients, we attempted to define allergenic relationships between diverse pollen species.MethodsSera from subjects were examined in direct IgE antibody binding experiments and by quantitative inhibition, protein blotting and adsorption and edition studies.ResultsSera from subjects diagnosed as allergic to white cypress pine. Italian cypress. ryegrass or birch pollen were shown to have IgE antibodies that reacted with pollens from these four species and from cocksfoot, couch grass, lamb's quarter, wall pellitory. olive, plantain and ragweed. These reactions were confirmed in protein blotting and adsorption and elution studies where numerous IgE‐binding bands were detected in all 11 different pollen extracts with sera from each of the different allergic categories, further evidence of allergenic (i.e. IgE‐binding crossreactivity between the different pollens was provided by inhibition studies in which clear‐cut inhibitions of IgE binding to the different pollen allergen discs were obtained with comparable amounts of the different pollen extracts.ConclusionWe conclude that the presence of pollen reactive IgE antibodies may not necessarily be a true reflection of sensitizing polle

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01107.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SummaryBackgroudEpithelial cells release cytokines and they probably contribute to chronic inflammation detected in bronchial asthma, rhinitis and nasal polyposis.ObjectivesTo investigate the effect of cultures on cytokine gene expression to compare epithelial cell cytokine release by both healthy nasal nucosa (HNM) and nasal polyps (NP), and the modulation by dexamethasone and to investigate which cytokines may promote eosinophil survival.MethodsEpithelials cells were cultured to confluence, human epithelial cell conditioned media generated with or without dexamethasone, and supernalanls measured by ELISA. Cytokine gene expression was investigated by reverse transcription‐polymerase chain reaction (RT‐PCR).ResultsFresh epithelial cells only expressed mRNA for intesleukin‐8 (IL‐8) and granulocyte macrophage‐colony stimulating factor (GM‐CSF) while cultured cells expressed mRNA for IL‐1β IL‐6, IL‐8, tumour necrosis factor‐α (TNFα) and GM‐CSF. Epithelial cells from NP significantly (P<0.05) released more IL‐8 (25431 ± 3163 pg/mL), and GM‐CSF (1229 ± 391 pg/mL) than those from HNM (18604 ± 1723pg/mL for IL‐8; and 611 ± 98 pg/mL for GM‐CSF), Dexamethasone 10 μM inhibited the release of all cytokines, this effect being similar (40 50%) in both HNM and NP. except for IL‐6 which was higher in HNM. Eosinophil survival induced by epithelial cell secretions from both HNM and NP was strongly blocked by GM‐CSF antibody while it was partially blocked by antibodies to TNFα and IL‐8.ConclusionsThese findings suggest that although epithelial cell culture procedures may upregulate cytokine gene expression, nasal polyps may represent a more active inflammatory tissue by releasing more cytokines than healthy nasal mucosa this release being inhibited by steroids; and that, in addition to GM‐CSF.other cytokines such as TNFo and IL‐8, may also be

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01108.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SummaryBackgroundCD4+and CD8+T‐lymphocytes are suggested to differentially affect airway inflammation in asthma. Agents which increase intracellular cAMP levels, such as PDE inhibitors, have been shown to diminish lymphocyte growth and differentiation, and to affect cytokine expression. Differences in the PDE isoenzyme profile between CD4+and CD8+cells might form a basis to differentially modify their functions by PDE inhibitors.ObjectiveThe study investigates and compares the PDE isoenzyme activity profiles of human peripheral blood CD4+and CD8+T‐lymphocytes.MethodsCD4+and CD8+T‐lymphocytes were purified (>98%) from peripheral blood mononuclear cells by negative selection. PDE isoenzyme activity profiles were investigated using PDE isoenzyme selective inhibitors and activators.ResultsIn CD4+and CD8+ T‐lymphocyte homogenates, PDE IV and PDE III activities were the predominant PDE isoenzyme activities at 0.5μM cyclic nucleotide substrate concentrations. PDE IV was localized in the soluble fraction whereas PDE III was membrane bound. Low PDE I, II and V activities were detected. About 20% of total eAMP hydrolysing capacity at 0.5 μM cAMP was insensitive to PDE isoenzyme selective inhibitors and activators and therefore could not be assigned to PDE I‐IV. The PDE isoenzyme pattern was not different between CD4+and CDS+T‐lymphocytes. Moreover, representative inhibitors of PDE HI and IV activity inhibited cAMP hydrolysis in soluble fractions of both T‐lymphocyte subsets with similar potency. Enzyme kinetic analysis similarly did not reveal differences between CD4hand CD8+T‐lymphocytes.ConclusionNormal CD4+and CD8+T‐lymphocytes are likely to be equally sensitive targets for the effect

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01109.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SummaryBackgroundAlveolar macrophages and their precursors, the monocytes are involved in airway inflammation in asthma. An increase in intraceliular cAMP by PDE inhibitors is known to suppress macrophage and monocyte functions. A comparison of the PDE‐isoenzyine profiles of human alveolar macrophages from normal and atopic donors and of human peripheral blood monocytes might form a basis to differentially affect functions of these cells by PDE inhibitors.ObjectiveThe study compares the PDE isoenzyme activity profiles of human alveolar macrophages from normal and atopic asthmatic donors and human peripheral blood monocytes. In addition, the effect ofin vitromaturation of monocytes on their PDE isoenzyme profile is studied.MethodsMacrophages were purified (95‐97%) by adherence to plastic, and blood monocytes were purified (88%) by counter‐current elutriation. PDE isoenzyme activity profiles were investigated using isoenzyme selective inhibitors and activators.ResultsIn macrophages substantial PDE I activity, which was significantly higher than PDE IIF‐V activity was detected and PDE II was absent. PDE III was membrane‐bound whereas PDE I, IV and V were soluble. No difference was found between alveolar macrophages of normal donors and atopic asthmatics. Monocytes exclusively contained PDE IV but theirin vitromaturation led to a PDE isoenzyme profile similar to that of alveolar macrophages.ConclusionThese results indicate that human monocytes and alveolar macrophages are distinct targets for the effects of selective PDE inhibitors while alveolar macrophages from normal and atopic individuals appear to be equally

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01110.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

SummaryBackgroundIt is widely held thatin vitroT cell responses to allergens are more prominent in atopic than in normal individuals, though this conclusion is based upon culture techniques which fail to detect proliferative responses in a significant minority of atopies and many normals.Objectives:Study allergen‐specific proliferative responses of T cells cultured in serum‐free medium (SFM). Examine associations between atopic status, age and T cell reactivity.MethodsInitially, peripheral blood mononuclear cells were stimulated with allergens or antigens in SFM, and compared with cells cultured in RPMI + 10% fetal calf serum or human AB serum. Subsequently, T cell reactivity was studied in 34 adults (20–49 years), 27 children (2–13 years), and 19 infants (≤ 10 weeks) using SFM alone.ResultsCompared with serum‐supplemented medium, SFM enhanced net T cell proliferation, both in bulk culture and when cloning at limiting dilution. In many subjects, SFM unmasked T cell reactivity to allergens which was not otherwise evident, and lowered the threshold allergen levels required forin vitroT cell triggering. For most allergens, T cell proliferative responses did not differ between adults who had specific IgE, and those who did not. The most vigorous responses observed were to ubiquitous inhalant allergens, which stimulated T cells from close to 100% of adults and children, and over 60% of infants. In contrast, responses to the ‘vaccine’ antigen tetanus toxoid were completely absent in the latter age group, but present in the majority of adults and children.ConclusionsThese findings suggest that the extent of active T cell recognition of environmental allergens has been hitherto underestimated, and further that these responses may frequently be initiated in very early life. Additionally, these findings reinforce the notion that qualitative (as opposed to quantitative) variations in specific T cell reactivity ultimately determine allergen resp

ISSN:0954-7894    

DOI:10.1111/j.1365-2222.1995.tb01111.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY