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Ozone inhalation induces exacerbation of eosinophilic airway inflammation and hyperresponsiveness in allergen-sensitized mice.
Allergy. 2008 Apr; 63(4):438-46.A

Abstract

BACKGROUND

Ozone (O(3)) exposure evokes asthma exacerbations by mechanisms that are poorly understood. We used a murine model to characterize the effects of O(3) on allergic airway inflammation and hyperresponsiveness and to identify factors that might contribute to the O(3)-induced exacerbation of asthma.

METHODS

BALB/c mice were sensitized and challenged with Aspergillus fumigatus (Af). A group of sensitized and challenged mice was exposed to 3.0 ppm of O(3) for 2 h and studied 12 h later (96 h after Af challenge). Naive mice and mice exposed to O(3) alone were used as controls. Bronchoalveolar lavage (BAL) cellular and cytokine content, lung function [enhanced pause (P(enh))], isometric force generation by tracheal rings and gene and protein expression of Fas and FasL were assessed. Apoptosis of eosinophils was quantified by FACS.

RESULTS

In sensitized mice allergen challenge induced a significant increase of P(enh) and contractile force in tracheal rings that peaked 24 h after challenge and resolved by 96 h. O(3) inhalation induced an exacerbation of airway hyperresponsiveness accompanied by recurrence of neutrophils and enhancement of eosinophils 96 h after allergen challenge. The combination of allergen and O(3) exposure inhibited Fas and FasL gene and protein expression and eosinophil apoptosis and increased interleukin-5 (IL-5), granulocyte-macrophage-colony stimulating factor (GM-CSF) and G-CSF protein levels.

CONCLUSIONS

O(3) affects airway responsiveness of allergen-primed airways indirectly by increasing viability of eosinophils and eosinophil-mediated pathological changes.

Authors+Show Affiliations

Pulmonary, Allergy and Critical Care Division, Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104-3403, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18315731

Citation

Kierstein, S, et al. "Ozone Inhalation Induces Exacerbation of Eosinophilic Airway Inflammation and Hyperresponsiveness in Allergen-sensitized Mice." Allergy, vol. 63, no. 4, 2008, pp. 438-46.
Kierstein S, Krytska K, Sharma S, et al. Ozone inhalation induces exacerbation of eosinophilic airway inflammation and hyperresponsiveness in allergen-sensitized mice. Allergy. 2008;63(4):438-46.
Kierstein, S., Krytska, K., Sharma, S., Amrani, Y., Salmon, M., Panettieri, R. A., Zangrilli, J., & Haczku, A. (2008). Ozone inhalation induces exacerbation of eosinophilic airway inflammation and hyperresponsiveness in allergen-sensitized mice. Allergy, 63(4), 438-46. https://doi.org/10.1111/j.1398-9995.2007.01587.x
Kierstein S, et al. Ozone Inhalation Induces Exacerbation of Eosinophilic Airway Inflammation and Hyperresponsiveness in Allergen-sensitized Mice. Allergy. 2008;63(4):438-46. PubMed PMID: 18315731.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ozone inhalation induces exacerbation of eosinophilic airway inflammation and hyperresponsiveness in allergen-sensitized mice. AU - Kierstein,S, AU - Krytska,K, AU - Sharma,S, AU - Amrani,Y, AU - Salmon,M, AU - Panettieri,R A,Jr AU - Zangrilli,J, AU - Haczku,A, PY - 2008/3/5/pubmed PY - 2008/4/16/medline PY - 2008/3/5/entrez SP - 438 EP - 46 JF - Allergy JO - Allergy VL - 63 IS - 4 N2 - BACKGROUND: Ozone (O(3)) exposure evokes asthma exacerbations by mechanisms that are poorly understood. We used a murine model to characterize the effects of O(3) on allergic airway inflammation and hyperresponsiveness and to identify factors that might contribute to the O(3)-induced exacerbation of asthma. METHODS: BALB/c mice were sensitized and challenged with Aspergillus fumigatus (Af). A group of sensitized and challenged mice was exposed to 3.0 ppm of O(3) for 2 h and studied 12 h later (96 h after Af challenge). Naive mice and mice exposed to O(3) alone were used as controls. Bronchoalveolar lavage (BAL) cellular and cytokine content, lung function [enhanced pause (P(enh))], isometric force generation by tracheal rings and gene and protein expression of Fas and FasL were assessed. Apoptosis of eosinophils was quantified by FACS. RESULTS: In sensitized mice allergen challenge induced a significant increase of P(enh) and contractile force in tracheal rings that peaked 24 h after challenge and resolved by 96 h. O(3) inhalation induced an exacerbation of airway hyperresponsiveness accompanied by recurrence of neutrophils and enhancement of eosinophils 96 h after allergen challenge. The combination of allergen and O(3) exposure inhibited Fas and FasL gene and protein expression and eosinophil apoptosis and increased interleukin-5 (IL-5), granulocyte-macrophage-colony stimulating factor (GM-CSF) and G-CSF protein levels. CONCLUSIONS: O(3) affects airway responsiveness of allergen-primed airways indirectly by increasing viability of eosinophils and eosinophil-mediated pathological changes. SN - 1398-9995 UR - https://www.unboundmedicine.com/medline/citation/18315731/Ozone_inhalation_induces_exacerbation_of_eosinophilic_airway_inflammation_and_hyperresponsiveness_in_allergen_sensitized_mice_ L2 - https://doi.org/10.1111/j.1398-9995.2007.01587.x DB - PRIME DP - Unbound Medicine ER -