English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Chronic exposure to particulate matter < 2.5µ (PM 2.5 ) has been linked to cardiopulmonary disease. Tissue-resident (TR) alveolar macrophages (A Φ ) are long-lived, self-renew and critical to the health impact of inhalational insults. There is an inadequate understanding of the impact of PM 2.5  exposure on the nature/time course of transcriptional responses, self-renewal of A Φ , and the contribution from bone marrow (BM) to this population. Accordingly, we exposed chimeric (CD45.2/CD45.1) mice to concentrated PM 2.5  or filtered air (FA) to evaluate the impact on these end-points. PM 2.5  exposure for 4-weeks induced an influx of BM-derived monocytes into the lungs with no contribution to the overall TR-A Φ  pool. Chronic (32-weeks) PM 2.5  exposure on the other hand while associated with increased recruitment of BM-derived monocytes and their incorporation into the A Φ  population, resulted in enhanced apoptosis and decreased proliferation of TR-A Φ . RNA-seq analysis of isolated TR-A Φ  and BM-A Φ  from 4- and 32-weeks exposed mice revealed a unique time-dependent pattern of differentially expressed genes. PM 2.5  exposure resulted in altered histological changes in the lungs, a reduced alveolar fraction which corresponded to protracted lung inflammation. Our findings suggest a time-dependent entrainment of BM-derived monocytes into the A Φ  population of PM 2.5  exposed mice, that together with enhanced apoptosis of TR-A Φ  and reorganization of transcriptional responses, could collectively contribute to the perpetuation of chronic inflammation.

scientific reports

Differential contribution of bone marrow-derived infiltrating monocytes and resident macrophages to persistent lung inflammation in chronic air pollution exposure