Low Dose Carbon Black Nanoparticle Exposure Does Not Aggravate Allergic Airway Inflammation in Mice Irrespective of the Presence of Surface Polycyclic Aromatic Hydrocarbons.

Karina Lindner,Michael Stroebele,Sina Webering,Henning Bockhorn,Tanja Hansen,Heinz Fehrenbach,Peter König

doi:10.3390/nano8040213

Abstract

Exposure to exogenous noxae, such as particulate matter, can trigger acute aggravations of allergic asthma—a chronic inflammatory airway disease. We tested whether Carbon Black nanoparticles (CBNP) with or without surface polycyclic aromatic hydrocarbons (PAH) aggravate an established allergic airway inflammation in mice. In an ovalbumin mouse model, Printex®90 (P90), P90 coated with benzo[a]pyrene (P90-BaP) or 9-nitroanthracene (P90-9NA), or acetylene soot exhibiting a mixture of surface PAH (AS-PAH) was administered twice (70 µL, 100 µg/mL) during an established allergic airway inflammation. We analyzed the immune cell numbers and chemokine/cytokine profiles in bronchoalveolar lavages, the mRNA expressions of markers for PAH metabolism (Cyp1a1, 1b1), oxidative stress (HO-1, Gr, Gpx-3), inflammation (KC, Mcp-1, IL-6, IL-13, IL-17a), mucin synthesis (Muc5ac, Muc5b), the histology of mucus-producing goblet cells, ciliary beat frequency (CBF), and the particle transport speed. CBNP had a comparable primary particle size, hydrodynamic diameter, and ζ-potential, but differed in the specific surface area (P90 > P90-BaP = P90-9NA = AS-PAH) and surface chemistry. None of the CBNP tested increased any parameter related to inflammation. The unmodified P90, however, decreased the tracheal CBF, decreased the Muc5b in intrapulmonary airways, but increased the tracheal Muc5ac. Our results demonstrated that irrespective of the surface PAH, a low dose of CBNP does not acutely aggravate an established allergic airway inflammation in mice.

Highlights

Asthma is a common airway disease with more than 241 million prevalent cases worldwide in 2013 [1]
We showed that Carbon Black nanoparticles (CBNP) coated with polycyclic aromatic hydrocarbons (PAH) had only minor pro-inflammatory effects in healthy animals in vivo [21]
CBNP might exert different responses in individuals suffering from lung diseases, such as allergic asthma, and might result in the induction of an acute asthma exacerbation

Summary

Introduction

Asthma is a common airway disease with more than 241 million prevalent cases worldwide in 2013 [1]. During an acute asthmatic response, the sufferer’s breathing is limited by an obstruction of the airway induced by smooth muscle constriction and mucus plugs in the airway lumen [2,3,4]. Asthmatic responses are associated with increased mucus secretion from goblet cells, epithelial injury, cellular infiltrations of immune cells, hyperplasia of smooth muscles, and deposition of excess collagen [2,5,6,7,8]. Because an exacerbation may require an emergency department visit or the hospitalization of the patient, asthma exacerbations are the main cost drivers of this chronic airway disease. Asthma exacerbations can be triggered by a variety of factors including air pollution [10]

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Conclusion