Repeated Exposure to Wood Smoke Alters Pulmonary Gene and Metabolic Profiles
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA994474 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25258428.fastq.gz | Fastqsanger.gz | |||
| SRR25258429.fastq.gz | Fastqsanger.gz | |||
| SRR25258430.fastq.gz | Fastqsanger.gz | |||
| SRR25258431.fastq.gz | Fastqsanger.gz | |||
| SRR25258432.fastq.gz | Fastqsanger.gz |
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Project description:This study tested the hypothesis that a medicinal plant, Vasaka, typically consumed as a tea to treat respiratory malaise, could protect airway epithelial cells (AECs) from wood smoke particle-induced damage and prevent pathological mucus expression. Wood/biomass smoke is a common pneumotoxic air pollutant that activates transient receptor potential ankyrin 1 (TRPA1) and causes endoplasmic reticulum (ER) stress and AEC damage. This stimulates epidermal growth factor receptor and mucin 5AC (MUC5AC) production by AECs. Mucus normally protects the airways, but excessive MUC5AC production can obstruct airflow and cause respiratory distress. Vasaka tea pre- and co-treatment dose-dependently inhibited MUC5AC mRNA induction in cells treated with wood smoke particles. This correlated with TRPA1 inhibition, an attenuation of ER stress, and AEC damage/death, among other effects. Induction of mRNA for Anterior Gradient 2 (AGR2), an ER chaperone/disulfide isomerase required for MUC5AC production, and TRP vanilloid-3 (TRPV3), a gene that suppresses ER stress and wood smoke particle-induced cell death, were also attenuated. Variable inhibition of TRPA1, ER stress, and MUC5AC mRNA induction was observed using selected chemicals identified in Vasaka tea including vasicine, vasicinone, apigenin, 9-oxoODE, and 9,10-EpOME. 9,10-EpOME and apigenin were the most cytoprotective and mucosuppressive. Cytochrome P450 1A1 mRNA was also induced by Vasaka tea and wood smoke particles. Inhibition of CYP1A1 enhanced ER stress and MUC5AC mRNA expression, suggesting a role in producing protective oxylipins in stressed cells. The results provide mechanistic insights and support for the purported benefits of Vasaka tea in treating lung inflammatory conditions, raising the possibility of further development as a preventative therapy.
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Project description:Chronic obstructive pulmonary disease (COPD) has the highest increased risk due to household air pollution arising from biomass fuel burning. However, knowledge on COPD patho-mechanisms is mainly limited to tobacco smoke exposure. In this study, a repeated direct wood smoke (WS) exposure was performed using normal- (bro-ALI) and chronic bronchitis-like bronchial (bro-ALI-CB), and alveolar (alv-ALI) lung mucosa models at air-liquid interface (ALI) to assess broad toxicological end points. The bro-ALI and bro-ALI-CB models were developed using human primary bronchial epithelial cells and the alv-ALI model was developed using a representative type-II pneumocyte cell line. The lung models were exposed to WS (10 minutes/exposure; 5-exposures over 3-days; n=6-7 independent experiments). Sham exposed samples served as control. WS composition was analyzed following passive sampling. Cytotoxicity, total cellular reactive oxygen species (ROS) and stress responsive NFkB were assessed by flow cytometry. WS exposure induced changes in gene expression were evaluated by RNA-seq (p≤0.01) followed by pathway enrichment analysis. Secreted levels of proinflammatory cytokines were assessed in the basal media. Non-parametric statistical analysis was performed. 147 unique compounds were annotated in WS of which 42 compounds have inhalation toxicity (9 very high). WS exposure resulted in significantly increased ROS in bro-ALI (11.2%) and bro-ALI-CB (25.7%) along with correspondingly increased NFkB levels (bro-ALI: 35.6%; bro-ALI-CB: 18.1%). A total of 1262 (817-up and 445-down), 329 (141-up and 188-down), and 102 (33-up and 69-down) genes were differentially regulated in the WS-exposed bro-ALI, bro-ALI-CB, and alv-ALI models respectively. The enriched pathways included the terms acute phase response, mitochondrial dysfunction, inflammation, oxidative stress, NFkB, ROS, xenobiotic metabolism of AHR, and chronic respiratory disorder. The enrichment of the ‘cilium’ related genes was predominant in the WS-exposed bro-ALI (180-up and 7-down). The pathways primary ciliary dyskinesia, ciliopathy, and ciliary movement were enriched in both WS-exposed bro-ALI and bro-ALI-CB. Interleukin-6 and tumor necrosis factor-α were reduced (p<0.05) in WS-exposed bro-ALI and bro-ALI-CB.
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