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J L Devalia

Publications and source records attributed to J L Devalia.

At least 37 records · Page 2Linked to original sources
PubMed1998

The effect of diesel exhaust particles on cell function and release of inflammatory mediators from human bronchial epithelial cells in vitro.

Animal studies have reported that diesel exhaust particles (DEP), which constitute an important fraction of particulate air pollution, lead to inflammation and/or damage of the airways. To investigate the mechanisms underlying DEP-induced airway disease in humans, we have cultured human bronchial epithelial cells (HBEC) from surgically obtained bronchial explants and investigated the effects of purified DEP on the permeability and ciliary beat frequency (CBF) of HBEC, and on the release of inflammatory mediators from these cells. Exposure to 10-100 microg/ml DEP and a filtered solution of 50 microg/ml DEP significantly increased the electrical resistance of the cultures, reaching a maximum of 200% over baseline after 6 h incubation with 100 microg/ml DEP. In contrast, movement of 14C-labeled bovine serum albumin across cell cultures was not significantly altered by incubation of HBEC with DEP. Exposure to 50 microg/ml DEP, filtered DEP solution, and 100 migrog/ml DEP significantly attenuated the CBF of these cells by 51%, 33%, and 73%, respectively, from baseline after 24 h incubation. Similarly, 50 microg/ml DEP, filtered DEP solution, and 100 microg/ml DEP significantly increased the release of interleukin-8 from 12.9 pg/microg cellular protein to 41.6, 114.9, and 44.3 pg/microg cellular protein, respectively, after 24 h incubation. The release of granulocyte-macrophage colony stimulating factor (GM-CSF) and soluble intercellular adhesion molecule-1 (sICAM-1) was also significantly increased after exposure for 24 h to 50 microg/ml DEP (GM-CSF from 0.033 pg/microg cellular protein to 0.056 pg/mug cellular protein and sICAM-1 from 7.2 pg/microg cellular protein to 12.5 pg/microg cellular protein). These results suggest that exposure of HBEC to DEP may lead to adverse functional changes and release of proinflammatory mediators from these cells, and that these effects may influence the development of airway disease.

Adult↗
PubMed1997

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.

BACKGROUND: Recent studies have suggested that airway epithelial cells of atopic and nonatopic individuals may differ in their ability to produce proinflammatory cytokines. METHODS: We have cultured human nasal epithelial cells (NECs) as confluent explant cultures from nasal biopsy specimens of well-characterized nonatopic normal volunteers without rhinitis (n = 8), atopic volunteers without rhinitis (n = 9), and atopic patient volunteers with rhinitis (n = 10) and measured the amounts of IL-1 beta, IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and RANTES released spontaneously into the culture medium by these cells in vitro. NECs from patients with allergic rhinitis were cultured from biopsy specimens obtained on two different occasions, during and after the pollen season. RESULTS: In general, NECs from atopic individuals released significantly greater amounts of IL-1 beta, IL-8, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and RANTES than NECs from nonatopic individuals. IL-8 was released in greatest quantity and IL-1 beta in lowest quantity, regardless of whether the NECs were derived from atopic or nonatopic volunteers. Of the atopic individuals, NECs of atopic patients with rhinitis naturally exposed to pollen released greater quantities of all these cytokines, compared with NECs of atopic patients with rhinitis and atopic patients without rhinitis who were not exposed to allergen. CONCLUSIONS: These results suggest that NECs of atopic individuals, who are genetically predisposed to upper airway disease, release increased amounts of proinflammatory cytokines and that natural exposure to allergen enhances the release of these cytokines, exacerbating the symptoms of allergic disease.

Adolescent↗
PubMed1997

Mechanisms of pollution-induced airway disease: in vitro studies in the upper and lower airways.

Evidence from both epidemiological and laboratory-based studies suggests that increased exposure to liquid petroleum and gas-derived air pollutants [nitrogen dioxide (NO2), ozone, and respirable particulate matter] may play a role in the clinical manifestation of both allergic and non-allergic airway disease. The mechanisms and cell types involved in pollutant-mediated effects in the airways, however, are not clear. In vitro studies have suggested that human fibroblasts, B-lymphocytes, alveolar macrophages, and epithelial cells/cell lines may be involved. Studies of fibroblasts and macrophages have demonstrated that exposure to ozone results in decreased cell viability and increased release of pro-inflammatory mediators from macrophages. Similarly, studies of B-lymphocytes have demonstrated that exposure to diesel exhaust particles (DEP) enhances the synthesis of immunoglobulin E by these cells. The airway epithelial cells have received the greatest attention in mechanistic studies of air pollution-induced airway disease and suggest that these cells are likely to play a pivotal role in the pathogenesis of airways disease. Various studies have demonstrated that exposure of nasal or bronchial epithelial cells to NO2, ozone, and DEP results in significant synthesis and release of pro-inflammatory mediators, including eicosanoids, cytokines, and adhesion molecules. Additionally, evidence suggests that epithelial cells of atopic individuals release significantly greater amounts of cytokines such as granulocyte-macrophage colony stimulating factor (GM-CSF), interleukin-6 (IL-6), IL-8, and regulated on activation, normal T-cell expressed and secreted (RANTES), on exposure to NO2 and ozone. Studies investigating the biological relevance of epithelial cell-derived pro-inflammatory mediators have shown that these enhance eosinophil chemotaxis and eosinophil adherence to endothelial cells, suggesting that pollution-induced inflammation of the airways is likely to be influenced by modulation of epithelial synthesis and release of these mediators.

Air Pollutants↗
PubMed1997

Allergen-irritant interaction and the role of corticosteroids.

Studies of exposure to air pollutants, such as ozone and nitrogen dioxide (NO2) +/- sulphur dioxide (SO2), have demonstrated that these agents, either individually or in combination, increase the airway response of both asthmatics and allergic rhinitics to inhaled allergen. Other studies have demonstrated that exposure to these pollutants significantly increased the levels of eosinophil cationic protein (ECP) in the nasal secretions of both asthmatics and allergic rhinitics, suggesting that pollutants may prime eosinophils for subsequent activation by allergen. More recently, our studies have demonstrated that treatment with inhaled corticosteroids, such as fluticasone propionate, significantly attenuated pollution+ allergen-induced release of ECP in allergic rhinitics. Although the mechanisms underlying the potentiating effects of pollutants on allergen-induced changes in the airways of allergic individuals are not fully understood, in vitro studies have suggested that airway epithelial cells may play an important role, since they can synthesize a variety of cytokines and adhesion molecules which influence the activity of eosinophils and other inflammatory cells. Studies of nasal epithelial cells cultured from biopsies of atopic rhinitic and atopic non-rhinitic individuals have shown that they constitutively release significantly greater quantities of pro-inflammatory cytokines than nasal epithelial cells of non-atopic individuals, and that the release of these cytokines is greater from cells of atopic rhinitics during the pollen season. Furthermore, exposure of the cells of rhinitics to ozone led to an even greater release of these cytokines, and this effect was attenuated by treatment with fluticasone propionate and beclomethasone dipropionate.

Adrenal Cortex Hormones↗
PubMed1997

New insights into the understanding of asthma.

The prevalence of asthma is increasing, despite better understanding of its pathogenesis and improved treatments. During the past 10 years, the perception of asthma has shifted from a disease primarily characterized by altered smooth muscle function to one mainly characterized by chronic inflammation. This article reviews the evidence supporting the relationship of inflammation in both the upper and lower airways, focusing on intermittent seasonal disease as well as on the more chronic and severe forms of asthma, including that associated with aspirin intolerance. It also presents evidence to support a pivotal role for the epithelial cell, together with the mast cell and the eosinophil, in initiating and maintaining inflammation in the upper and lower airways.

Air Pollutants↗
PubMed1997

Effect of corticosteroids on release of RANTES and sICAM-1 from cultured human bronchial epithelial cells, induced by TNF-alpha.

We have recently demonstrated that human bronchial epithelial cells can synthesise and release several inflammatory mediators, including the factor regulated on activation, normal T-cell expressed and secreted (RANTES) and soluble intercellular adhesion molecule-1 (sICAM-1), which influence the activity of eosinophils, and may, therefore play a role in the aetiology of asthma. In this study we investigated whether corticosteroids could influence the release of these proinflammatory mediators from human bronchial epithelial cells. Human bronchial epithelial cells were cultured to confluence as explant cultures, and incubated in the presence of 50 ng x mL(-1) tumour necrosis factor-alpha (TNF-alpha) +/- 0-10(-4) M of either fluticasone propionate (FP), beclomethasone dipropionate (BDP), or hydrocortisone (HC) for 24 h. The culture medium was collected and analyzed for RANTES and sICAM-1, by enzyme-linked immunosorbent assay (ELISA), and the cells were analysed for total protein. The TNF-alpha significantly increased the release both of RANTES and sICAM-1 (63.0 fg RANTES x microg(-1) protein; p<0.05; 8.8 pg sICAM-1 x microg(-1) protein; p<0.02), when compared with untreated cells (10.3 fg RANTES x microg(-1) protein; 2.6 pg sICAM-1 x microg(-1) cellular protein). The TNF-alpha-induced release both of RANTES and sICAM-1 occurred in a time-dependent manner, and was maximal by 24 h incubation. FP 10(-6)-10(-4) M significantly attenuated the TNF-alpha-induced release both of RANTES and sICAM-1. In contrast, 10(-4) M BDP or HC significantly attenuated the release of only sICAM-1. These results suggest that corticosteroids may prevent airway inflammation by downregulating the synthesis and/or release of proinflammatory mediators from bronchial epithelial cells. Furthermore, fluticasone propionate may be more efficacious than beclomethasone dipropionate or hydrocortisone in this respect.

Administration, Topical↗
PubMed1997

The effect of nedocromil sodium on human airway epithelial cell-induced eosinophil chemotaxis and adherence to human endothelial cell in vitro.

Although some studies have shown that long-term treatment of asthmatics with nedocromil sodium can reduce airway hyperresponsiveness and improve symptoms and lung function, the mechanisms underlying its effects are not well understood. We have investigated the effect of nedocromil sodium on eosinophil chemotaxis, eosinophil adherence to human endothelial cells and release of soluble intercellular adhesion molecule-1 (sICAM-1) from endothelial cells, induced by conditioned medium collected from cultured human bronchial epithelial cells. Conditioned medium significantly increased eosinophil chemotaxis from a baseline median value of 2.1 (range 1.9-4.5) cells-high power field(-1) (HPF) to 10.5 (range 7.8-12.3) cells-HPF(-1) (p<0.05). Similarly, conditioned medium significantly increased eosinophil adherence to endothelial cells from a baseline value of 9 (range 8-12)% to 23 (range 21-30)% (p<0.05). Nedocromil sodium, at 10(-5) M concentration, significantly attenuated the eosinophil chemotaxis and adherence induced by conditioned medium. Conditioned medium also significantly increased the release of sICAM-1 from endothelial cells, from a baseline value of 11.5 (range 8.1-15.4) pg x microg(-1) protein to 67.6 (range 55.6-73.5) pg x microg(-1) protein (p<0.05). This was significantly attenuated by anti-tumour necrosis factor-alpha (TNF-alpha), anti-interleukin-1beta (IL-1beta) and 10(-5) M nedocromil sodium. These findings suggest that human bronchial epithelial cell-derived mediators may potentiate eosinophil activity, and that this can be modulated by nedocromil sodium, suggesting a possible mechanism underlying its anti-inflammatory effect.

Anti-Asthmatic Agents↗
PubMed1996

Air pollutants and respiratory hypersensitivity.

Epidemiological evidence suggests that an increase in liquid petroleum derived pollutants is associated with exacerbation of allergic airway disease, and that the effects of pollution may occur 1-2 days later. Laboratory based studies have demonstrated that the pollutants responsible for the adverse effects on respiratory health include nitrogen dioxide (NO2), sulphur dioxide (SO2), ozone (O3) and respirable particulates (PM10). More recently, studies of asthmatic individuals exposed to O3, NO2 and a combination of NO2 and SO2 have indicated that these agents increase the airway responsiveness of these individuals to inhaled allergen, and that this effect may be maximal 24 h after exposure to the pollutants. Studies investigating the putative mechanisms underlying the effects of these pollutants suggest that exposure to these agents may lead to perturbation of the airway epithelium and release of pro-inflammatory mediators from the epithelial cells, which then influence the activity of inflammatory cells, such as eosinophils.

Adult↗
PubMed1996

Airway response of asthmatic subjects to inhaled allergen after exposure to pollutants.

BACKGROUND: Recent studies have suggested that air pollutants resulting from vehicle exhaust emissions and burning of fossil fuels, either in combination or individually, may enhance the airway response of asthmatic subjects to inhaled allergen. It was hypothesised that the airway response to inhaled allergen after exposure to a combination of 400 ppb nitrogen dioxide (NO2) and 200 ppb sulphur dioxide (SO2) is increased 24-48 hours after exposure. METHODS: Thirteen mild atopic asthmatic volunteers were exposed for six hours to a single exposure of air and three exposures of the combination of 400 ppb NO2 + 200 ppb SO2 in randomised order, and then challenged with increasing concentrations of Dermatophagoides pteronyssinus allergen either immediately after exposure to air, or immediately, 24 hours or 48 hours after exposure to the combination of the two pollutants, until a 20% fall in forced expiratory volume in one second (FEV1) was recorded. RESULTS: Exposure to 400 ppb NO2 + 200 ppb SO2 significantly decreased the dose of D pteronyssinus allergen required to produce a 20% fall in FEV1 (PD20FEV1) at all times after exposure when compared with air. The mean percentage changes in allergen PD20FEV1 immediately, 24 hours, and 48 hours after exposure to 400 ppb NO2 + 200 ppb SO2 were -37% (95% confidence intervals (CI) -50 to -23), -63% (CI -75 to -51), and -49% (CI -75 to -28.8), respectively, when compared with the PD20FEV1 after air exposure and were significant at all time points studied. The allergen PD20FEV1 at 24 hours after exposure to the combination of the two pollutants was also found to be significantly lower when compared with that immediately after exposure to the two pollutants. CONCLUSION: These results demonstrate that exposure to a combination of NO2 and SO2, at concentrations which can be encountered during episodes of increased outdoor and indoor air pollution, enhances the airway response to inhaled allergen in asthmatic subjects. This effect persists over a period of 24-48 hours and is maximal 24 hours after exposure to these air pollutants.

Adult↗
PubMed1996

Expression of RANTES by human bronchial epithelial cells in vitro and in vivo and the effect of corticosteroids.

Recent studies have demonstrated that RANTES, a member of the CC chemokine family affecting monocytes, T cells, basophils, and eosinophils, is expressed by several cell types. To investigate whether human bronchial epithelial cells can also express this chemokine, we investigated human bronchial epithelial cells for their ability to synthesize RANTES, both in vitro and in vivo. Additionally, we investigated the effect of treatment for 4 mo with inhaled corticosteroids on the expression of RANTES in these cells in vivo. Human bronchial epithelial cells cultured from surgical tissue expressed the mRNA for RANTES and synthesized RANTES, as demonstrated by polymerase chain reaction and immunocytochemical staining and enzyme-linked immunosorbent assay, respectively. Incubation of the cultures with 50 ng/ml of tumor necrosis factor-alpha (TNF-alpha) significantly increased the release of RANTES into culture medium after 18 to 48 h of incubation, an effect that was abolished by treatment of the cultures with anti-TNF-alpha antibody. RANTES was also expressed in the bronchial epithelium in vivo, as indicated by positive immunocytochemical staining of bronchial biopsy tissues obtained from mild asthmatic patients before and after treatment with 500 micrograms of inhaled beclomethasone dipropionate (BDP) twice daily or matched placebo for 4 mo. Quantitation, by color image analysis, of the percentage of epithelium staining for RANTES showed that treatment with BDP decreased the expression of RANTES in the bronchial epithelium from 17.12% to 4.22% (P < 0.05). The numbers of EG2-staining cells in the epithelium were also reduced, from 790.1/mm2 to 203.3/mm2 (geometric mean; P < 0.01), after BDP treatment. These results suggest that human bronchial epithelial cells are capable of synthesizing RANTES and may therefore play an important role in the development of inflammation in allergic airways disease. Furthermore, corticosteroids may prevent airway inflammation by downregulating the expression of proinflammatory cytokines in the bronchial epithelium.

Administration, Inhalation↗
PubMed1996

Bacterial-induced release of inflammatory mediators by bronchial epithelial cells.

This review focuses on bacterial induction and release of inflammatory cytokines and adhesion molecules by human bronchial epithelial cells, with special reference to Haemophilus influenzae, a pathogen commonly associated with chronic bronchitis. Studies investigating the mechanisms underlying bacterial colonization of the airways and bacterial-induced chronic airway inflammation have suggested that these are likely to involve localization of bacteria to the site(s) of infection in the respiratory tract and induction of a local airway inflammation resulting in the initiation of epithelial damage. We have hypothesized that the gross airway epithelial damage observed in chronic infective lung disease is an indirect consequence of proteolytic enzymes and toxic oxygen radicals generated by large numbers of neutrophils infiltrating the airways. Furthermore, the infiltration and activation of the neutrophils is a consequence of increased release of proinflammatory mediators from the host respiratory epithelium, induced by bacterial products, such as endotoxin. This hypothesis is based on studies which have demonstrated that the concentrations of circulating cytokines, such as interleukin (IL)-8 and tumour necrosis factor-alpha (TNF-alpha), which have profound effects on neutrophil activity, are increased in endotoxaemia and that airway epithelial cells are a rich source of these cytokines. Support for this hypothesis is provided by studies of cultured human bronchial epithelial cells incubated either in the absence or presence of purified endotoxin preparations from nontypable and type b H. influenzae strains which have demonstrated that these endotoxins lead to significantly increased expression and/or release of proinflammatory mediators, including IL-6, IL-8, TNF-alpha and intercellular adhesion molecule-1 (ICAM-1). Treatment of the cells with steroids can downregulate the expression and/or release of these inflammatory mediators. Additionally, these studies have demonstrated that culture medium collected from endotoxin-treated cultures, 24 h after treatment, significantly increases neutrophil chemotaxis and adhesion to human endothelial cells in vitro.

Bacterial Proteins↗
PubMed1996

Ozone-induced mediator release from human bronchial epithelial cells in vitro and the influence of nedocromil sodium.

Although animal and human studies have demonstrated that ozone inhalation leads to airway epithelial inflammation and damage, the underlying mechanisms are not fully understood. We cultured human bronchial epithelial cells as explant cultures and investigated the effect of 6 h of exposure to 0-500 parts per billion (ppb) O3 with or without 10(-5) M nedocromil sodium on: 1) epithelial cell membrane integrity; and 2) release of inflammatory cytokines and soluble intercellular adhesion molecule-1 (sICAM-1), as assessed by enzyme-linked immunosorbent assay (ELISA). O3 exposure led to significant epithelial cell damage at concentrations of 10-500 ppb O3, as indicated by increased release of [51Cr]-labelled sodium chromate. At concentrations of 10-100 ppb, O3 induced maximal release of interleukin-8 (IL-8), granulocyte/macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-alpha (TNF-alpha) and sICAM-1. The IL-8 and GM-CSF release increased significantly from 5.64+/-0.58 and 0.04+/-0.03 pg x microg(-1) cellular protein, respectively, from control cells exposed to air, to 20.16+/-2.56 and 0.20+/-0.04 pg x microg(-1) cellular protein, respectively, from cells exposed to 50 ppb O3. 10(-5) M nedocromil sodium significantly attenuated the O3-induced release of both IL-8 and GM-CSF (p<0.01). The TNF-alpha and sICAM-1 increases after exposure to 10-50 ppb O3, were also abrogated by treatment of the cells with 10(-5) M nedocromil sodium (p<0.05). Similarly, the antioxidant, glutathione, at concentrations of 400-600 microM, significantly reduced the O3-induced release of IL-8 (p<0.05). In conclusion, these studies indicate that ambient concentrations of ozone may induce airway inflammation, through release of proinflammatory mediators from airway epithelial cells. This effect may be inhibited both by the anti-inflammatory drug, nedocromil sodium, and the naturally occurring antioxidant glutathione.

Adult↗
PubMed1996

Nedocromil sodium and airway inflammation in vivo and in vitro.

We conducted a series of studies investigating the antiinflammatory effects of nedocromil sodium, with particular reference to its effects on human bronchial epithelial cells and eosinophils in vitro and on eosinophils in vivo. Nedocromil sodium produced a dose-related inhibition of ozone-induced IL-8 release from human bronchial epithelial cells and also attenuated the release of granulocyte macrophage colony-stimulating factor, tumor necrosis factor-alpha, and soluble intercellular adhesion molecule 1. The culture medium from human bronchial epithelial cell cultures, containing the proinflammatory cytokines IL-8, granulocyte macrophage colony-stimulating factor, "regulated on activation, normal T expressed and secreted," IL-1 beta, and tumor necrosis factor-alpha, increased eosinophil chemotaxis and eosinophil adhesion to cultured human endothelial cells. The chemotaxis and increased adhesion were blocked in the presence of nedocromil sodium. The drug also abrogated the epithelial cell dysfunction (assessed as ciliary beat frequency) induced by the presence of activated eosinophils and blocked the release of eosinophil cationic protein from the eosinophils. We also conducted a double-blind placebo-controlled study of the effects of regular albuterol 200 micrograms or nedocromil sodium 4 mg, both given four times daily for 16 weeks, on inflammatory cell numbers in bronchial biopsy and bronchoalveolar lavage samples. Assessed in terms of total and activated eosinophils in biopsy samples, inflammation decreased with nedocromil sodium and was significantly different from a deterioration with albuterol, although neither of these changes was significantly different from that with placebo treatment. Levels of eosinophil cationic protein in bronchoalveolar lavage samples showed a similar trend.

Asthma↗
PubMed1995

Synthesis and secretion of procathepsin B and cystatin C by human bronchial epithelial cells in vitro: modulation of cathepsin B activity by neutrophil elastase.

Procathepsin B and cystatin C are found in human lung secretions. We investigated the capacity of human bronchial epithelial cells to synthesize and secrete these proteins. Immunoprecipitation of [35S]methionine-labeled proteins from cultured bronchial epithelial cell lysates, followed by denaturing gel electrophoresis and autoradiography, showed the presence of newly synthesized procathepsin B of M(r) 42,000; no mature form was detected. Cathepsin B in conditioned medium from epithelial cells was tagged with benzyloxycarbonyl-125I-tyrosyl-alanine-diazomethane before and after treatment of the medium with neutrophil elastase. Control medium again showed a predominant form of cathepsin B with a M(r) of 42,000, but upon treatment with neutrophil elastase this protein was converted to a M(r) of 38,000, similar to the active form previously found in lung secretions, and cathepsin B activity was generated. The medium also contained the cathepsin B inhibitor, cystatin C, but cystatins A, B, S, SN, SA, and kininogen were not detected. After removal of cystatin C from the medium, elastase was still required to activate procathepsin B. These results suggest that bronchial epithelial cells are a source of procathepsin B and cystatin C in lung secretions. Cleavage both of cystatin C and procathepsin B by neutrophil elastase is essential for the generation of cathepsin B activity in the medium.

Bronchi↗
PubMed1995

Effect of six-hour exposure to nitrogen dioxide on early-phase nasal response to allergen challenge in patients with a history of seasonal allergic rhinitis.

BACKGROUND: Recent studies have suggested that exposure to air pollutants may enhance the airway responsiveness of susceptible individuals to inhaled allergen. METHODS: To investigate the effect of exposure to nitrogen dioxide (NO2) on nasal airways resistance (NAR) and inflammatory mediators in nasal lavage fluid, eight subjects with a history of seasonal allergic rhinitis, who were tested out of season, were exposed in a randomized single-blind, crossover study to either air or 400 ppb NO2 for 6 hours. The changes in NAR and eosinophil cationic protein (ECP), mast cell tryptase (MCT), neutrophil myeloperoxidase (MPO), and interleukin-8 (IL-8) in nasal lavage fluid before and after exposure were evaluated. Another group of eight subjects with a history of seasonal allergic rhinitis were also randomized to exposure to air or 400 ppb NO2 for 6 hours and then challenged with allergen, before evaluation for changes in NAR and changes in ECP, MCT, MPO, and IL-8 in nasal lavage fluid. RESULTS: Exposure to air or NO2 did not alter either NAR or the levels of ECP, MCT, MPO, or IL-8 in nasal lavage fluid. Allergen challenge after exposure to both air and NO2 significantly (p < 0.05) increased levels of MCT, but not MPO and IL-8 in the nasal lavage fluid. In addition, allergen challenge after exposure to NO2 but not air, significantly increased levels of only ECP in nasal lavage fluid (p < 0.05). CONCLUSIONS: These results suggest that acute exposure to NO2 at concentrations found at the curbside in heavy traffic during episodes of pollution, may "prime" eosinophils for subsequent activation by allergen in individuals with a history of seasonal allergic rhinitis.

Adolescent↗