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Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts

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ABSTRACT

Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases inflammation in the lungs can be targeted and inhibited via p38 MAP kinase pathway.

No MeSH data available.


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Measurement of cell viability with different hardwood and softwood smoke extract concentrations. Human primary lung fibroblasts (n = 5) were stimulated with hardwood (A) and softwood (B) smoke extract (1%–10%) in 0.1% FBS/DMEM. Cell viability was measured using MTT assay at 24 h after stimulation. Data expressed as the percent of unstimulated fibroblasts and bars represent mean ± SEM. Statistical analysis was executed using one-way ANOVA with Tukey’s post-test. No significant differences were found.
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ijms-17-01403-f001: Measurement of cell viability with different hardwood and softwood smoke extract concentrations. Human primary lung fibroblasts (n = 5) were stimulated with hardwood (A) and softwood (B) smoke extract (1%–10%) in 0.1% FBS/DMEM. Cell viability was measured using MTT assay at 24 h after stimulation. Data expressed as the percent of unstimulated fibroblasts and bars represent mean ± SEM. Statistical analysis was executed using one-way ANOVA with Tukey’s post-test. No significant differences were found.

Mentions: To assess the potential toxicological effect of biomass smoke, cells were exposed to 1%–10% of hardwood and softwood smoke for 24 h stimulation. Cell viability was measured via MTT assay, and confirmed by trypan blue exclusion assays. We found a trend of decreasing number of viable cells with increasing concentrations of hardwood and softwood smoke extract stimulation (Figure 1). We then investigated lower concentrations (0.01%, 0.1%, and 1%) of hardwood and softwood smoke extract and found no toxic effects of biomass smoke extract by trypan blue exclusion assays (Figure 2A,B) and LDH assays (Figure 2C,D). Overall we observed no differences in the toxicity of hardwood and softwood smoke extract.


Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts
Measurement of cell viability with different hardwood and softwood smoke extract concentrations. Human primary lung fibroblasts (n = 5) were stimulated with hardwood (A) and softwood (B) smoke extract (1%–10%) in 0.1% FBS/DMEM. Cell viability was measured using MTT assay at 24 h after stimulation. Data expressed as the percent of unstimulated fibroblasts and bars represent mean ± SEM. Statistical analysis was executed using one-way ANOVA with Tukey’s post-test. No significant differences were found.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5037683&req=5

ijms-17-01403-f001: Measurement of cell viability with different hardwood and softwood smoke extract concentrations. Human primary lung fibroblasts (n = 5) were stimulated with hardwood (A) and softwood (B) smoke extract (1%–10%) in 0.1% FBS/DMEM. Cell viability was measured using MTT assay at 24 h after stimulation. Data expressed as the percent of unstimulated fibroblasts and bars represent mean ± SEM. Statistical analysis was executed using one-way ANOVA with Tukey’s post-test. No significant differences were found.
Mentions: To assess the potential toxicological effect of biomass smoke, cells were exposed to 1%–10% of hardwood and softwood smoke for 24 h stimulation. Cell viability was measured via MTT assay, and confirmed by trypan blue exclusion assays. We found a trend of decreasing number of viable cells with increasing concentrations of hardwood and softwood smoke extract stimulation (Figure 1). We then investigated lower concentrations (0.01%, 0.1%, and 1%) of hardwood and softwood smoke extract and found no toxic effects of biomass smoke extract by trypan blue exclusion assays (Figure 2A,B) and LDH assays (Figure 2C,D). Overall we observed no differences in the toxicity of hardwood and softwood smoke extract.

View Article: PubMed Central - PubMed

ABSTRACT

Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases inflammation in the lungs can be targeted and inhibited via p38 MAP kinase pathway.

No MeSH data available.


Related in: MedlinePlus