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.
Highlights
These were similar to wood smoke (WS) concentrations found at rural areas homes of people exposed throughout Mexico [11] and similar to our previous shortexposure and chronic models of exposure to WS in guinea pigs [12,13]
This study focused on analyzing pro-inflammatory mediators and the molewith the upregulation of the mRNAs of several inflammatory cytokines, matrix metalloproteinases (MMPs), and tissue inhibitors of metalloproteinases (TIMPs) cules involved in the extracellular matrix (ECM) remodeling induced by WS
With similar doses to indoor pollution measurements, acute exposure to WS induces the overexpression of some pro-inflammatory cytokines, gelatinases (MMP-2, and MMP-9), and TIMPs (TIMP-1 and TIMP-2) in bronchoalveolar lavages (BAL) and serum
Summary
One ambient air polluting source is the smoke derived from biomass combustion, especially wood smoke (WS) derived from domestic incineration and forest fires [1]. WS is a global poor health risk factor that can cause oxidative stress, inflammation, and remodeling of the extracellular matrix (ECM). WS can elicit several lung diseases, such as bronchitis, pneumonia, acute respiratory failure, chronic obstructive pulmonary disease (COPD), and various systemic diseases [2,3,4,5,6]. Exposure to biomass smoke by indoor air pollution is strongly associated with COPD in the long term [2,3]
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