Particles from wood smoke and road traffic differently affect the innate immune system of the lung

Abstract

The effect of particles from road traffic and wood smoke on the innate immune response in the lung was studied in a lung challenge model with the intracellular bacterium Listeria monocytogenes. Female Balb/cA mice were instilled intratracheally with wood smoke particles, particles from road traffic collected during winter (studded tires used; St+), and during autumn (no studded tires; St−), or diesel exhaust particles (DEP). Simultaneously with, and 1 or 7 days after particle instillation, 10⁵ bacteria were inoculated intratracheally. Bacterial numbers in the lungs and spleen 1 day after Listeria challenge were determined, as an indicator of cellular activation. In separate experiments, bronchoalveolar lavage (BAL) fluid was collected 4 h and 24 h after particle instillation. All particles tested reduced the numbers of bacteria in the lung 24 h after bacterial inoculation. When particles were given simultaneously with Listeria, the reduction was greatest for DEP, followed by St+ and St−, and least for wood smoke particles. Particle effects were no longer apparent after 7 days. Neutrophil numbers in BAL fluid were increased for all particle exposed groups. St+ and St− induced the highest levels of IL-1β, MIP-2, MCP-1, and TNF-α, followed by DEP, which induced no TNF-α. In contrast, wood smoke particles only increased lactate dehydrogenase (LDH) activity, indicating a cytotoxic effect of these particles. In conclusion, all particles tested activated the innate immune system as determined with Listeria. However, differences in kinetics of anti-Listeria activity and levels of proinflammatory mediators point to cellular activation by different mechanisms.

Acknowledgements

We thank Arja de Klerk (National Institute of Public Health and the Environment (RIVM), Department of Toxicology, Pathology and Genetics, Bilthoven, The Netherlands) for providing Listeria monocytogenes and Joseph K. H. Ma and Xuejun J. Yin (Shool of Pharmacy and School of Medicine, West Virginia University, Morgantowns, West Virginia, USA) for providing valuable information on the preparation of L. monocytogenes for animal infection. The authors acknowledge Anette Kocbach for planning and administering the particle sample collection and for the chemical and morphological analyses. We thank Trude Karin Olsen, åse Eikeset, Astri Grestad, Else-Carin Groeng, Bodil Hasseltvedt, and Berit A Stensby for excellent technical assistance. The endotoxin measurements provided by Randi Jacobsen are highly appreciated.

Declaration of interest: This work was funded by a grant from the Norwegian Academy of Science and Letters and Statoil (VISTA) (6141) and The Norwegian Institute of Public Health. The authors alone are responsible for the content and writing of the paper.