Late-phase Asthmatic Reaction to Inhaled Allergen Is Associated with Early Recruitment of Eosinophils in the Airways

Rossi, Giovanni A.; Crimi, Emanuele; Lantero, Sabina; Gianiorio, Piero; Oddera, Susanna; Crimi, Paolo; Brusasco, Vito

doi:10.1164/ajrccm/144.2.379

Cited by 106 publications

(68 citation statements)

References 5 publications

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“…There is also some evidence that NO 2 exposure leads to persistent neutrophilic infiltration in human airways (34) and to increased histamine release in histocultured human nasal mucosa (35). The inflammatory mechanisms of pollen and fungal allergens in allergic respiratory disease have also been described (36)(37)(38). Our finding of a divergence of association in the medication groups for aeroallergens is not unexpected and demonstrates the value of stratifying panel data.…”

Section: Discussionsupporting

confidence: 60%

Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use.

Delfino

Zeiger

Seltzer

et al. 2002

Environ Health Perspect

185

135

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Maxima of hourly data from outdoor monitors may capture adverse effects of outdoor particulate matter (PM) exposures in asthmatic children better than do 24-hr PM averages, which form the basis of current regulations in the United States. Also, asthmatic children on anti-inflammatory medications may be protected against the proinflammatory effects of air pollutants and aeroallergens. We examined strengths of pollutant associations with asthma symptoms between subgroups of asthmatic children who were on versus not on regularly scheduled anti-inflammatory medications, and tested associations for different particle averaging times. This is a daily panel study of 22 asthmatic children (9-19 years of age) followed March through April 1996 (1,248 person-days). They lived in nonsmoking households in a semirural area of Southern California within the air inversion mixing zone (range, 1,200-2,100 feet) with transported air pollution from urban areas of Southern California. The dependent variable derived from diary ordinal scores is episodes of asthma symptoms that interfered with daily activities. Minimum to 90th-percentile levels of exposures at the outdoor monitoring site were 12-63 microg/m(3) for 1-hr PM < 10 microm in aerodynamic diameter (PM(10)); 8-46 microg/m(3) for 8-hr PM(10); 7-32 microg/m(3) for 24-hr PM(10); 45-88 ppb for 1-hr O(3); 6-26 ppb for 8-hr NO(2); 70-4,714 particles/m(3) for 12-hr daytime fungi; and 12-744 particles/m(3) for 24-hr pollen. Data were analyzed with generalized estimating equations controlling for autocorrelation. There was no confounding by weather, day of week, or linear time trend. Associations were notably stronger in 12 asthmatic children who were not taking anti-inflammatory medications versus 10 subjects who were. Odds ratios (95% confidence intervals) for asthma episodes in relation to lag 0 minimum to 90th-percentile pollutant changes were, respectively, 1-hr maximum PM(10), 1.92 (1.22-3.02) versus 0.96 (0.25-3.69); 8-hr maximum PM(10), 1.68 (0.91-3.09) versus 0.75 (0.18-3.04); 24-hr average PM(10), 1.35 (0.82-2.22) versus 0.80 (0.24-2.69); 1-hr maximum O(3), 1.28 (0.75-2.17) versus 0.76 (0.24-2.44); 8-hr maximum NO(2), 1.91 (1.07-3.39) versus 1.08 (0.30-3.93); 12-hr fungi, 1.89 (1.24-2.89) versus 0.90 (0.35-2.30); 24-hr pollen, 1.90 (0.99-3.67) versus 0.85 (0.18-3.91). Pollutant associations were stronger during respiratory infections in subjects not on anti-inflammatory medications. Although lag 0 1-hr maximum PM(10) showed the strongest association, the most robust associations were for lag 0 and 3-day moving averages (lags 0-2) of 8-hr maximum and 24-hr mean PM(10) in sensitivity analyses testing for thresholds. Most pollutant effects were largely driven by concentrations in the upper quintile. The divergence of exposure-response relationships by anti-inflammatory medication use is consistent with experimental data on inflammatory mechanisms of airborne pollutants and allergens.

show abstract

Section: Discussionsupporting

confidence: 60%

Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use.

Delfino

Zeiger

Seltzer

et al. 2002

Environ Health Perspect

185

135

View full text Add to dashboard Cite

show abstract

“…A number of studies in humans and animals have examined the inflammatory responses to inhaled stimuli [26][27][28][29][30][31][32] and suggest that the nature of the stimulus may determine the type of cellular response in the airways. Inhalation of ozone [26] or the occupational sensitizing agent toluene diisocyanate [29] have been associated with increased numbers of neutrophils in bronchoalveolar lavage fluid.…”

Section: Discussionmentioning

confidence: 99%

“…Inhalation of ozone [26] or the occupational sensitizing agent toluene diisocyanate [29] have been associated with increased numbers of neutrophils in bronchoalveolar lavage fluid. Challenge with inhaled allergen [30,32] and the inflammatory response in patients with Western red cedar asthma [33] has been associated with increased numbers of eosinophils.…”

Section: Discussionmentioning

confidence: 99%

Airway structure and inflammatory cells in fatal attacks of asthma

Carroll¹,

Carello²,

Cooke³

et al. 1996

Eur Respir J

204

129

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Fatal attacks of asthma usually occur against a background of chronic persistent symptoms, presumably due to chronic airway inflammation and changes in airway wall structure. Death from asthma is usually attributed to excessive airway narrowing due to a combination of muscle spasm and mucous plugging. To test the hypothesis that airway wall structure and/or the inflammatory cell profile are related to the duration of a fatal attack of asthma, inflammatory cell profiles and airway structure were examined in cases of fatal asthma and related to the duration of the fatal attack.In transverse sections of large and small airways from subjects dying from asthma, the numbers of eosinophils, neutrophils and lymphomononuclear cells were counted. The amount of smooth muscle shortening, the areas of airway wall, smooth muscle, mucous gland and cartilage were measured. Cell counts, airway dimensions and muscle shortening were compared in cases dying within 2 h of the fatal attack (short duration) and those dying more than 5 h after the onset of the fatal attack (long duration).In cases with fatal attacks of short duration, the numbers of neutrophils and the mucous gland area were increased and the numbers of eosinophils were reduced compared to cases with fatal attacks of long duration. Lymphocyte numbers, airway wall thickness, the areas of smooth muscle and cartilage and the amount of smooth muscle shortening were similar in the two groups.These findings suggest fatal attacks of asthma may be triggered by an inflammatory stimulus and suggest that increased production of mucous may contribute to sudden death in such cases.

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“…Bronchoscopy and BAL were performed as described previously [14]. Briefly, after premedication with atropine (0.5 mg i.m.)…”

Section: Fibreoptic-bronchoscopy and Balmentioning

confidence: 99%

The repertoire of T-lymphocytes recovered by bronchoalveolar lavage from healthy nonsmokers

Burastero¹,

Borgonovo²,

Gaffi³

et al. 1996

Eur Respir J

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We reasoned that persistent exposure to a limited set of airborne antigens could drive the preferential expansion of single T-cell clones in the lower respiratory tract of normal individuals. To explore this issue, the normal human α/β T-cell receptor repertoire was studied in lung lymphocytes obtained by bronchoalveolar lavage (BAL) from the lumen of the lower respiratory tract.BAL T-cells obtained from five healthy volunteers were first analysed using polymerase chain reaction to amplify all known Vα and Vβ genes of the T-cell receptor. T-cells from peripheral blood were used as an internal control. Heteroduplex analysis of the amplified products was then performed, to assess the clonal composition of the repertoire of lung-versus blood-derived T-lymphocytes within each amplified variable gene family.In all subjects, the T-cell repertoire in the lung was largely as heterogeneous as peripheral blood in terms of clonal composition. This indicated lack of preferential expansion of single T-cell clones. A few T-cell clones were simultaneously expanded in blood and lung in all individuals within a limited number of Vβ (mean 2.4; range 2-4) and Vα (mean 1.6; range 1-3) genes. We also found that lung Tlymphocytes expressed all of the V gene families of the T-cell receptor that were expressed by peripheral blood T-cells.Our results indicate that T-cell clones in the lower respiratory tract of normal individuals are distributed according to a largely polyclonal pattern, which corresponds to that found in peripheral blood.

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Late-phase Asthmatic Reaction to Inhaled Allergen Is Associated with Early Recruitment of Eosinophils in the Airways

Cited by 106 publications

References 5 publications

Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use.

Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use.

Airway structure and inflammatory cells in fatal attacks of asthma

The repertoire of T-lymphocytes recovered by bronchoalveolar lavage from healthy nonsmokers

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