LPS Response Is Impaired by Urban Fine Particulate Matter.

Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM2.5 in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1ß, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1ß, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM2.5 exposure.

Air pollution impairs recovery and tissue remodeling in a murine model of acute lung injury.

Evidence regarding the impact of air pollution on acute respiratory distress syndrome (ARDS) is limited, and most studies focus on ARDS onset. Our study aimed to evaluate whether exposure to fine particulate matter interferes with lung recovery and remodeling in a murine model of acute lung injury. Forty-eight mice received nebulized LPS or the vehicle (controls). Blood, BALF, lungs and spleen were collected after 5 weeks of exposure to either PM2.5 (PM and LPS + PM group) or filtered air (control and LPS5w groups). Inflammatory cells and cytokines were assessed in the blood, BALF, lungs and spleen. Stereological analyses and remodeling assessments were performed by histology. The LPS + PM group showed increased BALF leukocytes, characterized by increased macrophages, increased IL-1ß and IL-6 levels, anemia and thrombocytopenia. Moreover, we also observed septal thickening, decreased alveolar air space total volume and, septa surface density. Finally, regarding tissue remodeling, we observed elastosis of the lung parenchyma, and unlike in the LPS5w group, we did not observe fibrosis in the LPS + PM group. In conclusion, the delayed inflammation resolution due to subchronic exposure to PM2.5 could be influenced by low systemic and local lymphocyte counts, which lead to impaired lung injury recovery and tissue remodeling.

Early and late pulmonary effects of nebulized LPS in mice: An acute lung injury model.

BACKGROUND AND OBJECTIVE: Acute respiratory distress syndrome (ARDS) has a high mortality rate of 35-46% depending on its severity. Animal models are crucial to better understand the pathophysiology of diseases, including ARDS. This study presents a feasible animal model of acute lung injury (ALI) using nebulized lipopolysaccharide (LPS) in a non-invasive approach, focusing on its short and long-term effects. METHODS: Mice received nebulized LPS or vehicle only (control group). Blood, BALF and lung tissue were collected 24 hours (LPS 24h) or 5 weeks (LPS 5w) after the nebulized LPS-induced lung injury. Inflammatory cytokines were assessed in the blood serum, BALF and lung tissue. Stereological analyses and remodeling changes were assessed by histology and immunohistochemistry at the specified time points. RESULTS: The LPS 24h group showed increased pro-inflammatory cytokine levels, intense cell influx, increased total septal volume, septal thickening and decreased surface density of the alveolar septa. The LPS 5w group showed persistent lung inflammation, septal thickening, increased total lung volume, accentuated collagen deposition, especially of collagen type I, and decreased MMP-2 protein expression. CONCLUSION: We present a feasible, reproducible and non-invasive nebulized-LPS animal model that allows the assessment of both the acute and late phases of acute lung injury. The presence of lung remodeling with collagen deposition after 5 weeks makes it useful to study the pathophysiology, complications, and possible therapeutic intervention studies that aim to understand and reduce pulmonary fibrosis in the late phases of ALI.

Estudo ecotoxicológico da nanopartícula de prata em Daphnia similis / Ecotoxicological study of silver nanoparticle on Daphnia similis

Objetivo ­Verificar a toxicidade da NPAg em organismos aquáticos por meio do ensaio de ecotoxicidade aguda. O aumento na produção e utilização das nanopartículas de prata (NPAg) em diversas áreas, tem provocado preocupação quanto aos impactos e riscos potenciais que estas podem causar ao meio ambiente. Métodos ­ O teste de ecotoxicidade aguda foi realizado seguindo a Norma Brasileira ABNT NBR 12713, utilizando como organismo-teste a Daphnia similis. A exposição dos organismos ocorreu em cinco concentrações de NPAg, durante 48 horas. O resultado de CE50, concentração do agente tóxico que causa imobilidade a 50% dos organismos expostos, da NPAg foi obtida pelo método estatístico de Trimmed Spearman-Karber. Resultados ­ A média da CE50 da NPAg obtidas nos três ensaios realizados foi de 4,70 µg L­1. Conclusão ­ De acordo com os resultados obtidos, a NPAg causou imobilidade a 50% dos organismos expostos na concentração de 4,70 µg L­1. Estudos devem ser continuados para melhor esclarecimento dos impactos no meio ambiente aquático.

Objective ­ To assess the toxicity of AgNP in aquatic organisms through acute ecotoxicity test. The increasing of silver nanoparticle (AgNP) production and use in several areas, has caused great concern about the potential impacts and risks that they can cause to the environment. Methods ­ The ecotoxicity tests were carried out according to the Brazilian Standard ABNT NBR 12713, using Daphnia similis as test-organisms. The organisms were exposed to five AgNP concentrations for a period of 48 hours. The AgNP EC50 result, concentration of the toxic agent which causes immobility to 50% of exposed organisms, was obtained by the statistical method of Spearman-Karber Trimmed. Results ­ The average of AgNP EC50 result from three performed tests was 4.70 µg L­1. Conclusion ­ According to the results, AgNP showed immobility to 50% of exposed organisms in the concentration of 4.70 µg L­1. Studies must be continued to better understand the impacts on the aquatic environment.