暴露于野火烟雾中的空气污染物和室内污染会导致肺部疾病。部分已知短期暴露于木烟(WS)会改变人基质金属蛋白酶(MMPs)的表达,炎性细胞因子,和金属蛋白酶(TIMPs)的组织抑制剂。因此,我们研究了在不同日期将豚鼠暴露于WS2和4个3小时的时间的影响。室内污染报告的每日颗粒含量是由60克松木产生的。我们分析了支气管肺泡灌洗(BAL)中的细胞谱和胶原蛋白含量。促炎细胞因子的mRNA表达,MMPs,并在肺组织中研究了TIMPs。在BAL和血清中分析细胞因子和明胶分解活性。结果表明,总细胞,巨噬细胞,中性粒细胞,BAL中的胶原蛋白增加,而中性粒细胞和淋巴细胞减少。TGF-β1,TNF-α,IFN-γ,IL-1β,IL-6,IL-8,MMP-2,MMP-9,TIMP-1和TIMP-2在肺中上调,下调IL-12。TNF-α,IFN-γ,TGF-β1,IL-1β,IL-6和IL-8在BAL和血清中升高,降低IL-12。血清中明胶酶活性增加。因此,暴露于短期国内剂量的WS过表达的促炎细胞因子的豚鼠,MMPs,和TMPs。这些结果类似于在人类中报道的ECM重塑以及肺和全身性炎症。
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.