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Ultrafine but not fine particulate matter causes airway inflammation and allergic airway sensitization to co-administered antigen in mice

Authors

  • C. De Haar,

    1. Department of Immunotoxicology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
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    • 1Current address: Laboratory of Pediatrics, Division Gastroenterology and Nutrition, Erasmus MC, Rotterdam, The Netherlands.

  • I. Hassing,

    1. Department of Immunotoxicology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
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  • M. Bol,

    1. Department of Immunotoxicology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
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  • R. Bleumink,

    1. Department of Immunotoxicology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
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  • R. Pieters

    1. Department of Immunotoxicology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands
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Correspondence:
Colin de Haar, Laboratory of Pediatrics, Division of Gastroenterology and Nutrition, Erasmus MC, Room Ee1571, Dr. Molewaterplein 50 3015, GE Rotterdam, The Netherlands.
E-mail: c.dehaar@erasmusmc.nl

Summary

Background Airborne particulate matter (PM) is an important factor associated with the enhanced prevalence of respiratory allergy. The PM adjuvant activity on allergic sensitization is a possible mechanism of action involved, and the induction of airway inflammation is suggested to be of importance in PM-induced adjuvant activity.

Objective Because differently sized PM have different toxic potentials, we studied the role of particle size in the induction of airway inflammation and allergic sensitization. This was done using fine (0.250 and 0.260 μm) and ultrafine (0.029 and 0.014 μm) titanium dioxide (TiO2) and carbon black particles (CBP) with known differences in airway toxicity.

Methods Mice were intranasally exposed to ovalbumin (OVA) alone or in combination with one of the different particles. The induction of airway inflammation and the immune adjuvant activity were studied in the lungs and lung-draining peribronchial lymph nodes (PBLN) at day 8. OVA-specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after OVA challenges (day 28).

Results When administered at the same total particle mass (200 μg), exposure to ultrafine TiO2 and CBP-induced airway inflammation, and had immune adjuvant activity. The latter was shown by increasing both the PBLN cell numbers and the production of OVA-specific T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-10 and IL-13). Whereas OVA-specific IgE and IgG1 levels in serum were only increased in animals exposed to the ultrafine TiO2, allergic airway inflammation could be detected in both ultrafine TiO2-and CBP-treated groups after challenges with OVA.

Conclusion Our data show that only the ultrafine particles, with a small diameter and a large total surface area/mass, cause airway inflammation and have immune adjuvant activity in the current model supporting the hypothesis that particle toxicity is site-dependent and related to adjuvant activity.

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