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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.


Related in: MedlinePlus

IL-6 (A) and IL-8 (B) induction from Hardwood and Softwood smoke exposure at lower concentrations. Human primary lung fibroblasts (n = 6) were stimulated with hardwood and softwood smoke extract (0.01%, 0.1% and 1%) in 0.1% FBS/DMEM for 24 h. Cell free supernatants were collected and IL-6 (A) and IL-8 (B) release was measured via ELISA. Data were expressed in pg/mL and bars represent mean ± SEM. Comparisons between IL-6/IL-8 release from control and different concentrations of hardwood and softwood smoke extract made by one-way ANOVA with Tukey’s post-test. Significance is represented as * p < 0.05, ** p < 0.01 vs. control, *** p < 0.001 vs. control.
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ijms-17-01403-f003: IL-6 (A) and IL-8 (B) induction from Hardwood and Softwood smoke exposure at lower concentrations. Human primary lung fibroblasts (n = 6) were stimulated with hardwood and softwood smoke extract (0.01%, 0.1% and 1%) in 0.1% FBS/DMEM for 24 h. Cell free supernatants were collected and IL-6 (A) and IL-8 (B) release was measured via ELISA. Data were expressed in pg/mL and bars represent mean ± SEM. Comparisons between IL-6/IL-8 release from control and different concentrations of hardwood and softwood smoke extract made by one-way ANOVA with Tukey’s post-test. Significance is represented as * p < 0.05, ** p < 0.01 vs. control, *** p < 0.001 vs. control.

Mentions: Cell free supernatants were collected from fibroblasts stimulated with hardwood and softwood smoke extract (0.01%, 0.1%, and 1%) and IL-6 and IL-8 release was assessed via ELISA. We found a significant increase of both IL-6 and IL-8 release from 1% hardwood and softwood smoke extract stimulation (Figure 3).


Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts
IL-6 (A) and IL-8 (B) induction from Hardwood and Softwood smoke exposure at lower concentrations. Human primary lung fibroblasts (n = 6) were stimulated with hardwood and softwood smoke extract (0.01%, 0.1% and 1%) in 0.1% FBS/DMEM for 24 h. Cell free supernatants were collected and IL-6 (A) and IL-8 (B) release was measured via ELISA. Data were expressed in pg/mL and bars represent mean ± SEM. Comparisons between IL-6/IL-8 release from control and different concentrations of hardwood and softwood smoke extract made by one-way ANOVA with Tukey’s post-test. Significance is represented as * p < 0.05, ** p < 0.01 vs. control, *** p < 0.001 vs. control.
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ijms-17-01403-f003: IL-6 (A) and IL-8 (B) induction from Hardwood and Softwood smoke exposure at lower concentrations. Human primary lung fibroblasts (n = 6) were stimulated with hardwood and softwood smoke extract (0.01%, 0.1% and 1%) in 0.1% FBS/DMEM for 24 h. Cell free supernatants were collected and IL-6 (A) and IL-8 (B) release was measured via ELISA. Data were expressed in pg/mL and bars represent mean ± SEM. Comparisons between IL-6/IL-8 release from control and different concentrations of hardwood and softwood smoke extract made by one-way ANOVA with Tukey’s post-test. Significance is represented as * p < 0.05, ** p < 0.01 vs. control, *** p < 0.001 vs. control.
Mentions: Cell free supernatants were collected from fibroblasts stimulated with hardwood and softwood smoke extract (0.01%, 0.1%, and 1%) and IL-6 and IL-8 release was assessed via ELISA. We found a significant increase of both IL-6 and IL-8 release from 1% hardwood and softwood smoke extract stimulation (Figure 3).

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 &le; 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 &le; 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