Leal Mayara Peres, Brochetti Robson Alexandre, Ignácio Aline, Câmara Niels Olsen Saraiva, da Palma Renata Kelly, de Oliveira Luis Vicente Franco, de Fátima Teixeira da Silva Daniela, Lino-Dos-Santos-Franco Adriana
Post Graduate Program in Biophotonics Applied to Health Sciences, University Nove de Julho (UNINOVE), São Paulo, Brazil.
Department of Immunology, University of São Paulo, São Paulo, Brazil.
Toxicol Rep. 2018 Apr 5;5:512-520. doi: 10.1016/j.toxrep.2018.03.016. eCollection 2018.
Environmental and Occupational pollution has been extensively studied because of its serious implications on the human health. Formaldehyde (FA) is a pollutant widely employed in several industries and also in anatomy, pathology and histology laboratories. Studies have shown the correlation between FA exposure and development or worsening of asthma. However, the effect of FA exposure on the pulmonary fibrosis (PF) is unknown. PF is a progressive and chronic lung disease with high incidence and considerable morbidity and mortality. Few studies have shown a worsening of PF after pollutants exposure such as ozone and nitrogen dioxide. Therefore, our objective was to assess the effects of FA on the PF. Male mice C57BL6 were treated or not with bleomycin (1,5 U/kg) and exposed or not to FA inhalation (0.92 mg/m, 1 h/day, 5 days/week during 2 weeks). Non-manipulated mice were used as control. Our data showed that FA exposure in fibrotic mice increased the number of granulocytes in the bronchoalveolar lavage followed by elevated levels of interleukin 1 beta and interleukin 17. In addition, FA exposure in fibrotic mice enhanced the gene expression of C-X-C motif chemokine ligand 1 (CXCL1) and tumor necrosis factor alpha (TNF-α) in the lung. We also showed an increase in the collagen production, while lung elastance was reduced. differences were found in the mucus production, oedema and interstitial thickening in the lung tissue of fibrotic mice after FA exposure. In conclusion our study showed that FA exposure aggravates the lung neutrophils influx and collagen production, but did not alter the lung elastance, mucus production, oedema and interstitial tickening. This work contributes to understand the effects of pollution in the development of PF.
由于环境和职业污染对人类健康有严重影响，因此已对其进行了广泛研究。甲醛（FA）是一种广泛应用于多个行业以及解剖学、病理学和组织学实验室的污染物。研究表明，接触FA与哮喘的发生或恶化之间存在关联。然而，FA暴露对肺纤维化（PF）的影响尚不清楚。PF是一种进展性慢性肺部疾病，发病率高，发病率和死亡率可观。很少有研究表明接触臭氧和二氧化氮等污染物后PF会恶化。因此，我们的目标是评估FA对PF的影响。对雄性C57BL6小鼠进行博来霉素（1.5 U/kg）处理或不处理，并使其吸入FA（0.92 mg/m³，每天1小时，每周5天，持续2周）或不吸入。未进行处理的小鼠用作对照。我们的数据表明，纤维化小鼠接触FA后，支气管肺泡灌洗中的粒细胞数量增加，随后白细胞介素1β和白细胞介素17水平升高。此外，纤维化小鼠接触FA后，肺中C-X-C基序趋化因子配体1（CXCL1）和肿瘤坏死因子α（TNF-α）的基因表达增强。我们还发现胶原蛋白生成增加，而肺弹性降低。接触FA后，纤维化小鼠肺组织中的黏液分泌、水肿和间质增厚存在差异。总之，我们的研究表明，接触FA会加剧肺中性粒细胞流入和胶原蛋白生成，但不会改变肺弹性、黏液分泌、水肿和间质增厚。这项工作有助于了解污染在PF发展中的作用。
