Effects of formaldehyde exposure on the development of pulmonary fibrosis induced by bleomycin in mice. (2018)

• Record Type: Journal Article
• Authors: 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
• Is Part Of: Toxicology reports. Volume 5(2018)
• Page Start: 512
• Page End: 520
• Publication Date: 2018
• Subjects: Formaldehyde exposure -- Pulmonary fibrosis -- Lung inflammation -- Cytokines -- Lung elastance -- Collagen production; Toxicology -- Periodicals; Clinical toxicology -- Periodicals; Drug-Related Side Effects and Adverse Reactions; Hazardous Substances; Poisoning; Toxicology; Electronic journals; Periodicals; Periodicals; 571.9505
• DOI: 10.1016/j.toxrep.2018.03.016
• Languages: English
• ISSNs: 2214-7500

Abstract

Graphical abstract: Highlights: FA exposure aggravates the development of PF. FA exposure intensifies the collagen production into the lung worsening the PF. FA exposure exacerbates the lung cellular recruitment by CXCL1 and IL-17 mechanisms-involved. Abstract: 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 3, 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. No 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.