Effect of chronic PM exposure on gene expression in the mouse lung tissue
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ABSTRACT:
PROVIDER: PRJNA987717 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25031530.fastq.gz | Fastqsanger.gz | |||
| SRR25031531.fastq.gz | Fastqsanger.gz | |||
| SRR25031532.fastq.gz | Fastqsanger.gz | |||
| SRR25031533.fastq.gz | Fastqsanger.gz | |||
| SRR25031534.fastq.gz | Fastqsanger.gz |
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Project description:To identify differentially expressed genes in the lung by chronic PM exposure, we isolated mRNAs from the lung tissue from FVB/N mice after 4-weeks repeated intratracheal PM treatment
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Project description:Chronic exposure to ambient particulate matter <2.5µ (PM2.5) has been linked to cardiopulmonary disease. Tissue-resident (TR) alveolar macrophages (AΦ) are long lived, self-renew and critical to the health impact of inhalational insults. There is inadequate understanding of the impact of PM2.5 exposure on nature/time course of transcriptional responses and the proliferation/maintenance of AΦ including the contribution from bone marrow (BM) over chronic time periods. We investigated the effects of exposure to real-world concentrated PM2.5 or filtered air (FA) in chimeric (CD45.2/CD45.1) mice. Here, we show that PM2.5 exposure induces an influx of BM-derived monocytes to lungs at 4-weeks, with no contribution to TR-AΦ population. Chronic (32-weeks) PM2.5 exposure resulted in enhanced apoptosis (Annexin V+) and decreased proliferation (BrdU+) of TR-AΦ and presence of BM-AΦ in inflamed lungs. RNA-seq analysis of flow sorted TR-AΦ and BM-AΦ from 4 and 32-weeks exposed mice, revealed a unique time dependent pattern of differentially expressed genes, with PM2.5 exposure with a pro-inflammatory bias. PM2.5 exposure resulted in pulmonary fibrosis and reduced alveolar fraction which corresponded to protracted lung inflammation. Our findings suggest a time dependent PM2.5 entrainment of a BM-derived monocytes infiltration into PM2.5 exposed lungs with an inflammatory phenotype, that together with enhanced apoptosis of TR-AΦ and pro-inflammatory polarization may contribute to perpetuation of chronic inflammation and lung fibrosis.
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