Ramos Carlos, Cañedo-Mondragón Rebeca, Becerril Carina, González-Ávila Georgina, Esquivel Ana Laura, Torres-Machorro Ana Lilia, Montaño Martha
Laboratorio 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.
Laboratorio de Oncología Biomédica, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Calzada de Tlalpan 4502, Colonia Belisario Domínguez Sección XVI, Alcaldía Tlalpan, Mexico City 14080, Mexico.
Toxics. 2021 Sep 20;9(9):227. doi: 10.3390/toxics9090227.
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.
暴露于野火烟雾和室内污染中的空气污染物会引发肺部疾病。短期暴露于木烟(WS)中,已知会部分改变人类基质金属蛋白酶(MMPs)、炎性细胞因子和金属蛋白酶组织抑制剂(TIMPs)的表达。因此,我们研究了在不同日期将豚鼠暴露于WS中两个和四个三小时时间段的影响。室内污染报告的颗粒物每日含量由60克松木产生。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。研究了肺组织中促炎细胞因子、MMPs和TIMPs的mRNA表达。分析了BAL和血清中的细胞因子和明胶酶活性。结果显示,BAL中的总细胞、巨噬细胞、中性粒细胞和胶原蛋白增加,而中性粒细胞和淋巴细胞减少。肺中转化生长因子-β1(TGF-β1)、肿瘤坏死因子-α(TNF-α)、干扰素-γ(IFN-γ)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)、金属蛋白酶组织抑制剂-1(TIMP-1)和金属蛋白酶组织抑制剂-2(TIMP-2)上调,白细胞介素-12下调。BAL和血清中的TNF-α、IFN-γ、TGF-β1、IL-!β、IL-6和IL-8增加,白细胞介素-12减少。血清中的明胶酶活性增加。因此,暴露于短期家用剂量WS的豚鼠促炎细胞因子、MMPs和TIMPs过表达。这些结果与人类报告的细胞外基质重塑以及肺部和全身炎症相似。