A comparison of cytokine release from epithelial cells cultured from nasal biopsy specimens of atopic patients with and without rhinitis and nonatopic subjects without rhinitis (original) (raw)
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Cytokine secretion in nasal mucus of normal subjects and patients with allergic rhinitis
Biomedicine & Pharmacotherapy, 2003
Allergic rhinitis is regulated by the local production and release of several cytokines. The levels of Th2 cytokines IL-4, IL-6, IL-10 and the Th1 cytokine IFN-c were studied in nasal mucus from 30 subjects with allergic rhinitis and 45 non-atopic healthy controls. In this study a sampling technique for collecting nasal mucus, well tolerated by the subjects and with a minimal stimulation of the mucosa, was performed. The cytokine concentrations in nasal mucus samples were detected and quantitated by a new paramagnetic particle-based immunofluorescent assay system more sensitive than the conventional ELISA techniques. The new technique showed reliable values of the measured parameters. The nasal mucus from allergic patients contained significantly higher concentrations of IL-4 (25.5 ± 3.6 pg/ml; P < 0.001) and IL-10 (1300 ± 190 pg/ml; P < 0.05) compared to the nasal mucus from control subjects (15.2 ± 2.3 and 532 ± 28 pg/ml, respectively, for IL-4 and IL-10). No significant modification in IFN-c levels of allergic patients was found when compared to control group (respectively, 19.9 ± 3.3 vs. 25.7 ± 5.1 pg/ml; P > 0.05). Moreover, the allergic patients showed lower levels of IL-6 concentrations in the nasal mucus compared to control subjects (64.8 ± 9.1 vs. 129.0 ± 18.1 pg/ml; P = 0.0099). These data can be interpreted by the hypothesis that in response to environmental allergens there is a preferential Th2 polarity by activated CD4+ T cells and that the cytokines IL-6 and IL-10 have, respectively, an important anti-inflammatory and counterregulatory action in the pathogenesis of allergic rhinitis.
Regulation of Proinflammatory Cytokines in Seasonal Allergic Rhinitis
International Archives of Allergy and Immunology, 1999
Background: Mediators and cytokines have been demonstrated to be released due to nasal allergen exposure in sensitized subjects, but little is known about the release of cytokines and their antagonists under natural conditions. Methods: Mediators – histamine, eosinophilic cationic protein (ECP), leukotrienes (LT) C4/ D4/E4 – and cytokines – interleukin (IL)–1β, IL–8, IL–1 receptor antagonist (ra) – were measured in nasal secretions throughout the grass pollen season (6 visits) and for 6 weeks thereafter (3 visits) in patients with seasonal allergic rhinitis (n = 13) and compared to controls (n = 12). A second study was performed comparing nasal secretions of 13 subjects allergic to house dust mite to 8 controls. Results: Compared to controls, leukotrienes and ECP were significantly elevated at nearly all time points in and postseason in the allergic group. Whereas IL–1β was significantly elevated throughout the study period, IL–1ra was significantly decreased from visit 1 to 3. IL–8...
Allergen‐induced cytokine secretion in atopic and non‐atopic asthmatic children
Pediatric allergy …, 2003
induced cytokine secretion in atopic and non-atopic asthmatic children, 2003, Pediatric Allergy and Immunology, (14), 5, 345-350. which has been published in final form at: http://dx.Running title: Allergen induced cytokines in asthmatic children Malin F Böttcher -1 -Titel: Allergen induced cytokine secretion in atopic and non-atopic asthmatic children Journal: Pediatr Allergy Immunol
Scandinavian Journal of Immunology, 1998
Gabrielsson S, Söderlund A, Paulie S, Rak S, van der Pouw Kraan TCTM, Troye-Blomberg M. Increased Frequencies of Allergen-Induced Interleukin-13-Producing Cells in Atopic Individuals During the Pollen Season. Scand J Immunol 1998;48:429-435 We have reported previously that allergen-specific serum IgE levels were correlated with allergen-induced interleukin (IL)-4 in type I allergic individuals. Here, we wanted to investigate whether IL-13, another switch factor for IgE, was induced by allergen in vitro and if so, whether this was correlated with the elevated serum IgE-levels seen in atopic individuals, and whether the cytokine profile changed during pollen season. Peripheral blood mononuclear cells from 14 atopic and 14 healthy individuals collected out of the pollen season were incubated in vitro with allergens (birch or timothy) and the number of IL-4, IL-13, IL-10 and IFN-g producing cells was determined by ELISPOT. In response to the specific allergen, IL-13-producing cells were seen in allergic but not in healthy individuals. The number of IL-13-producing cells was significantly correlated with the allergen-specific serum IgE levels. When the allergic individuals were tested during the pollen season, the number of allergen-specific IL-4-and IL-13-producing cells, as well as serum levels of specific IgE, increased. The IL-13 increase seen in ELISPOT was confirmed by a RT-PCR assay. No seasonal changes were seen in response to purified protein derivative (PPD) or the mitogen PHA. During the pollen season, the IL-4 and IL-13 responses were highly correlated. Taken together, our results support the roles of both IL-13 and IL-4 in the regulation of allergen-specific IgE levels in atopic individuals.
Influence of interleukin-8 challenge in the nasal mucosa in atopic and nonatopic subjects
American Journal of Respiratory and Critical Care Medicine, 1994
lnterleukin-B (IL-B) is a major cytokine in the recruitment of neutrophils (polymorphonuclear leukocytes) to areas of inflammation. It also activates T lymphocytes and cytokine-primed basophils and eosinophils and therefore may be implicated as an effector in allergic inflammation. IL-B has also been identified as a mediator in such inflammatory pulmonary conditions as cystic fibrosis, allergen challenge, and sarcoidosis. To investigate the bioactivity of IL-B in humans, we examined the effects of nasal challenge with human recombinant IL-B in a double-blind placebo-controlled crossover study in which nasal resistance and rhinitic symptoms were monitored for 4 h after challenge. Cellular infiltration was quantified on differentially stained nasal smears obtained at hourly intervals. Cellular responses caused by in vivo priming were assessed by a comparison of atopic and nonatopic patient groups. A significant neutrophilic infiltrate in smear samples was observed in all patients challenged with IL-B from 12 ± 4% (mean ± SEM) at baseline to 60 ± 6% after 4 h; placebo challenge resulted in an increase in neutrophils to 30 ± 4% (p < 0.04). Additionally, a significant increase in cumulative eosinophil recruitment occurred over the challenge period. Nasal resistance was significantly increased 10 min after instillation of IL-B in all subjects compared with placebo, but there was no difference between atopic and nonatopic subjects. Nasal rhinitic symptoms were also increased in all subjects receiving IL-B compared with placebo. In a further study in 19 subjects, nasal biopsy was performed 3 h after IL-B or placebo challenge. Significantly increased neutrophil infiltration was observed following IL-B challenge compared with placebo challenge (32.4 ± 10.0 and 7.2 ± 2.0 cells/rnrns, respectively; p <0.037, ttest). We conclude that IL-B may be an important cytokine that contributes to rhinitic symptomatology and to both neutrophil and eosinophil influx in the respiratory mucosa.
The Immunology of Asthma and Allergic Rhinitis
Rhinosinusitis, 2019
The immune system is a complex collection of cells, tissues, and chemical mediators positioned throughout the body, whose primary purpose is to protect us against infection. However, its function is not only fundamental in protection from infectious disease but also provides aberrant response in allergens such as with asthma and allergic rhinitis. Allergic diseases like asthma and allergic rhinitis are characterized by a distinct type of inflammatory response, driven by immunoglobulin E (IgE)-dependent mechanisms. In asthma and allergic rhinitis, the inflammatory response is mediated by interaction of several immune cells (monocytes, lymphocytes, and polymorphonuclear cells) and cellular chemical mediators. In particular, atopic allergic response leads to destruction of multiple target cells such as epithelial, parenchymal and vascular and connective tissue of the airways. In addition, in inflammatory response in asthma and allergic rhinitis, sensory nerves are sensitized, leading to clinical manifestations. Sneezing and coughing are hypersensitivity responses of sensory nerves in allergic rhinitis and asthma, respectively. Similarly, nasal congestion and discharge in allergic rhinitis are due to vasodilatation that leads to plasma exudates as well as mucous secretion. The allergic inflammatory response is regulated by several transcription factors, particularly nuclear factor-κb (NF-κB), GATA-3 protein 3, and GATA binding protein.
Mucosal Immunology, 2016
Non-invasive mucosal sampling (nasosorption and nasal curettage) was used following nasal allergen challenge with grass pollen in subjects with allergic rhinitis, in order to define the molecular basis of the late allergic reaction (LAR). It was found that the nasal LAR to grass pollen involves parallel changes in pathways of type 2 inflammation (IL-4, IL-5 and IL-13), inflammasome-related (IL-1b), and complement and circadian-associated genes. A grass pollen nasal spray was given to subjects with hay fever followed by serial sampling, in which cytokines and chemokines were measured in absorbed nasal mucosal lining fluid, and global gene expression (transcriptomics) assessed in nasal mucosal curettage samples. Twelve of 19 subjects responded with elevations in interleukin (IL)-5, IL-13, IL-1b and MIP-1b/CCL4 protein levels in the late phase. In addition, in these individuals whole-genome expression profiling showed upregulation of type 2 inflammation involving eosinophils and IL-4, IL-5 and IL-13; neutrophil recruitment with IL-1a and IL-1b; the alternative pathway of complement (factor P and C5aR); and prominent effects on circadian-associated transcription regulators. Baseline IL-33 mRNA strongly correlated with these late-phase responses, whereas a single oral dose of prednisone dose-dependently reversed most nasal allergen challenge-induced cytokine and transcript responses. This study shows that the LAR to grass pollen involves a range of inflammatory pathways and suggests potential new biomarkers and therapeutic targets. Furthermore, the marked variation in mucosal inflammatory events between different patients suggests that in the future precision mucosal sampling may enable rational specific therapy.
Thorax, 1996
Background -Bronchial challenge with allergen causes a specific form of airways inflammation consisting of an influx of neutrophils, eosinophils, and T cells. Because the relevance of the challenge model to clinical asthma is uncertain, the cellular changes that occur in the lungs of asthmatic subjects during natural seasonal allergen exposure were investigated. Methods -Seventeen grass pollen sensitive asthmatic subjects with previously reported seasonal exacerbations of asthma kept records of symptoms and underwent fibreoptic bronchoscopy with bronchoalveolar lavage (BAL) and endobronchial biopsy before and during the peak of the grass pollen season. The BAL cells were analysed for differential cell counts and by flow cytometry for T cell subsets and surface activation markers. The biopsy samples were processed into glycol methacrylate resin and immunohistochemical analysis was performed for mast cells, activated eosinophils, T cells and interleukin 4 (IL-4), a cytokine with a pivotal role in allergen-induced inflammation. Results -In the pollen season there was an increase in T lymphocyte activation in the BAL fluid as identified by increased expression of interleukin 2 receptor (IL-2R). In the submucosa these changes were paralleled by an increase in CD4 + T cells. By contrast, the numbers of metachromatic cells in BAL fluid staining with toluidine blue were reduced, possibly because of degranulation following allergen stimulation. In keeping with mast cell activation, the number of mucosal mast cells staining for secreted IL-4 increased during the season. In comparison with the period shortly before the onset of the season, all but two subjects experienced an asthma exacerbation which followed the rise in pollen counts but, compared with the period preceding the first bronchoscopic examination, asthma symptoms were not increased during the pollen season. Conclusions -The data suggest that natural allergen exposure, leading to a clinical exacerbation of asthma, may induce an inflammatory response involving T cells, mast cells and eosinophils. The relationship between allergen exposure, cellular infiltration and activation, and clinical symptoms appears to be complex, with factors other than allergen also contributing to asthmatic activity. (Thorax 1996;51:575-581)
Bull Exp Biol Med, 2019
Plant lipid transfer proteins and homologues of the main birch pollen allergen Bet v 1 are involved in the development of allergic reactions of varying severity to plant foods and pollen. In this study, the sera from patients with tree and weed pollen allergies in the Moscow region were examined. The levels of IL-4, IL-5, IL-9, IL-10, IL-13, IL-17A, IFNγ, TNFα, and TNFβ cytokines were determined in the sera of patients with specific IgE antibodies to Bet v 1 and Pru p 3 allergens. It was confirmed that patients with pollen allergy are often characterized by Th2 response of the immune system, though other mechanisms of allergy development occurred in some cases. The data obtained demonstrate the necessity of detailed analysis of the individual mechanism of allergic reactions and patient-centered approach to the personalized allergy treatment.