Abstract

Background: Ambient particulate matter (PM) exposure has been shown to increase the risks of respiratory diseases and to contribute to the substantial worldwide burden of respiratory infections. However, the immune response to inhaled PM remains largely unexplored. Aim: We studied the effects of urban coarse PM on the pulmonary immunologic homeostasis. Methods: Male mice were exposed to urban coarse PM in a ventilated inhalation chamber for 3 and 15 days at a concentration relevant to episodic elevation peak of air pollution. Then the characteristics of PM-induced inflammation were assessed by flow cytometry and real-time PCR. Results: Acute and chronic exposures to urban coarse PM led to different immune patterns in the lung compartment. The acute phase was associated to the recruitment of neutrophils and activated alveolar macrophages. The chronic phase was characterized by the influx of activated conventional T cells whereas invariant natural killer T (iNKT) cells were recruited during both phases. Moreover, genes involved in anti-microbial responses, such as Reg3g, Lcn-2, Lyz and Slpi were downregulated in the lungs after acute PM exposure, whereas they were going back to baseline or slightly increased after chronic exposure. Independently of the time course, exposure to PM, leads to a decrease in IL-1b expression. Conclusion: This study provided a characterization of immunologic profiles in lungs following acute and chronic exposure to a realistic dose of PM. It suggested new mechanistic insights which should be further explored, especially the involvement of iNKT cells in pulmonary response to PM inhalation and the effects of PM exposure on the susceptibility to pulmonary infections.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.