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

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.


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Measurement of IL-6 production from hardwood (A) and softwood (B) smoke exposure and RV-16 infection. Primary human lung fibroblasts (n = 4) were stimulated with hardwood and softwood smoke extract at 0.1% and 1% concentration alone, RV-16 infection alone (MOI = 1), or both and incubated for 24 h. Unstimulated fibroblasts were also measured for IL-6 constitutive release. Supernatants were collected for IL-6 concentration via ELISA. Data expressed as pg/mL. Statistical analysis was executed using two-way ANOVA with Sidak’s post-test.
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ijms-17-01403-f005: Measurement of IL-6 production from hardwood (A) and softwood (B) smoke exposure and RV-16 infection. Primary human lung fibroblasts (n = 4) were stimulated with hardwood and softwood smoke extract at 0.1% and 1% concentration alone, RV-16 infection alone (MOI = 1), or both and incubated for 24 h. Unstimulated fibroblasts were also measured for IL-6 constitutive release. Supernatants were collected for IL-6 concentration via ELISA. Data expressed as pg/mL. Statistical analysis was executed using two-way ANOVA with Sidak’s post-test.

Mentions: Since epidemiological evidence suggests an interaction between biomass smoke and viral infection, we modelled this interaction in vitro. Fibroblasts were stimulated with biomass smoke extract initially (0.1% or 1%) and the infected with RV-16. As expected, hardwood and softwood smoke extract, and RV-16 alone, induced IL-6 and IL-8 release. Interestingly, RV increased IL-8 (Figure 4), but not IL-6 production (Figure 5) in both hardwood and softwood smoke exposed fibroblasts. In cells first infected with RV and then stimulated with biomass smoke extract, cytokine induction was not greater in comparison to RV alone.


Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts
Measurement of IL-6 production from hardwood (A) and softwood (B) smoke exposure and RV-16 infection. Primary human lung fibroblasts (n = 4) were stimulated with hardwood and softwood smoke extract at 0.1% and 1% concentration alone, RV-16 infection alone (MOI = 1), or both and incubated for 24 h. Unstimulated fibroblasts were also measured for IL-6 constitutive release. Supernatants were collected for IL-6 concentration via ELISA. Data expressed as pg/mL. Statistical analysis was executed using two-way ANOVA with Sidak’s post-test.
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Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037683&req=5

ijms-17-01403-f005: Measurement of IL-6 production from hardwood (A) and softwood (B) smoke exposure and RV-16 infection. Primary human lung fibroblasts (n = 4) were stimulated with hardwood and softwood smoke extract at 0.1% and 1% concentration alone, RV-16 infection alone (MOI = 1), or both and incubated for 24 h. Unstimulated fibroblasts were also measured for IL-6 constitutive release. Supernatants were collected for IL-6 concentration via ELISA. Data expressed as pg/mL. Statistical analysis was executed using two-way ANOVA with Sidak’s post-test.
Mentions: Since epidemiological evidence suggests an interaction between biomass smoke and viral infection, we modelled this interaction in vitro. Fibroblasts were stimulated with biomass smoke extract initially (0.1% or 1%) and the infected with RV-16. As expected, hardwood and softwood smoke extract, and RV-16 alone, induced IL-6 and IL-8 release. Interestingly, RV increased IL-8 (Figure 4), but not IL-6 production (Figure 5) in both hardwood and softwood smoke exposed fibroblasts. In cells first infected with RV and then stimulated with biomass smoke extract, cytokine induction was not greater in comparison to RV alone.

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