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Published on: October 22, 2020
Short-Term Exposure to Wood Smoke Increases the Expression of Pro-Inflammatory Cytokines, Gelatinases, and TIMPs in
Carlos Ramos1, Rebeca Cañedo-Mondragón1, Carina Becerril1
1Laboratorio de Biología Celular, Departamento de Investigación en Fibrosis Pulmonar, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Calzada de Tlalpan 4502, Colonia Belisario Domínguez Sección XVI, Alcaldía Tlalpan, Mexico City 14080, Mexico.
Abstract:
Exposure to air pollutants in wildfire smoke and indoor pollution causes lung diseases. Short-term exposure to wood smoke (WS) is partially known to alter the expression of human matrix metalloproteinases (MMPs), inflammatory cytokines, and tissue inhibitors of metalloproteinases (TIMPs). Accordingly, we investigated the effect of exposing guinea pigs to WS for two and four three-hour periods on different days. The daily content of particles reported by indoor pollution was produced by 60 g of pinewood. We analyzed the cell profile and collagen content in bronchoalveolar lavages (BAL). The mRNA expression of pro-inflammatory cytokines, MMPs, and TIMPs was studied in lung tissue. Cytokines and gelatinolytic activity were analyzed in BAL and serum. The results showed that total cells, macrophages, neutrophils, and collagen increased in BAL, whereas neutrophils and lymphocytes decreased. TGF-β1, TNF-α, IFN-γ, IL-1β, IL-6, IL-8, MMP-2, MMP-9, TIMP-1, and TIMP-2 were upregulated in lungs, downregulating IL-12. TNF-α, IFN-γ, TGF-β1, IL-1β, IL-6, and IL-8 were increased in BAL and serum, decreasing IL-12. Gelatinase activity was increased in serum. Thus, guinea pigs exposed to short-term domestic doses of WS overexpressed pro-inflammatory cytokines, MMPs, and TIMPs. These results are similar to ECM remodeling and pulmonary and systemic inflammation reported in humans.
Insights
Short-term exposure to wood smoke (WS) in guinea pigs increased inflammatory markers and matrix metalloproteinases (MMPs) in lungs and blood. These findings suggest WS contributes to lung disease and extracellular matrix remodeling similar to human responses.
Area of Science:
- Environmental Health
- Toxicology
- Pulmonary Medicine
Background:
- Wildfire smoke and indoor pollution are significant air pollutants linked to lung diseases.
- Short-term wood smoke (WS) exposure is known to affect matrix metalloproteinases (MMPs), inflammatory cytokines, and tissue inhibitors of metalloproteinases (TIMPs).
Purpose of the Study:
- To investigate the effects of short-term wood smoke (WS) exposure on lung tissue and bronchoalveolar lavage (BAL) in guinea pigs.
- To analyze the expression of pro-inflammatory cytokines, MMPs, and TIMPs following WS exposure.
Main Methods:
- Guinea pigs were exposed to WS from burning pinewood for two and four 3-hour periods on separate days.
- Analysis included cell profiles, collagen content in BAL, mRNA expression in lung tissue, and cytokine and gelatinolytic activity in BAL and serum.
Main Results:
- WS exposure increased total cells, macrophages, neutrophils, and collagen in BAL, while decreasing neutrophils and lymphocytes.
- Upregulation of pro-inflammatory cytokines (TGF-β1, TNF-α, IFN-γ, IL-1β, IL-6, IL-8), MMPs (MMP-2, MMP-9), and TIMPs (TIMP-1, TIMP-2) was observed in lungs, with downregulation of IL-12.
- Elevated cytokines and increased gelatinase activity were found in BAL and serum.
Conclusions:
- Short-term domestic doses of WS induced overexpression of pro-inflammatory cytokines, MMPs, and TIMPs in guinea pigs.
- These responses mirror extracellular matrix remodeling and pulmonary/systemic inflammation observed in humans exposed to air pollutants.
