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2612360 
Journal Article 
Abstract 
Diesel exhaust particles modulate lung immune responses via stimulation of dendritic cells 
Provoost, S; Maes, T; Willart, MM; Joos, GF; Lambrecht, BN; Tournoy, KG 
2010 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
181 
A1029 
English 
is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Rationale: Exposure to diesel exhaust particles (DEP) increases allergic sensitisation and aggravates pulmonary inflammation. Dendritic cells (DC) are crucial in regulating lung immune responses. We hypothesize that DEP cause their effects through modulation of the pulmonary DC.

Methods: BALB/c mice were instilled with saline or 100 µg DEP (SRM 2975) on days 1, 4 and 7. The effects of DEP on the lung innate immune response, DC subset recruitment and maturation, DC migration to the mediastinal lymph nodes and subsequent T-cell response were examined with flow cytometry.

Results: Exposure to DEP induces a strong innate immune response in the lung with increased numbers of neutrophils and monocytes. We demonstrate that exposure to DEP also accumulates CD11b+DC and CD11b-DC in the lung and increases the CD86 maturation marker on these conventional DC, whereas plasmacytoid DC were not affected. Using fluorescently labeled ovalbumine, we further show that exposure to DEP enhances the antigen-induced DC migration towards the mediastinal lymph nodes and that DEP themselves are transported to the mediastinal lymph nodes by a mechanism that involves CCR7. This results in an increased T-cell accumulation and effector differentiation in these mediastinal lymph nodes.

Conclusion: Exposure to DEP profoundly affects the biology of the pulmonary DC. Together, these findings suggest a mechanism by which DEP can increase allergic sensitisation and aggravate pulmonary inflammation. 
American Thoracic Society 2010 International Conference 
New Orleans, LA 
May 14-19, 2010