LPS Response Is Impaired by Urban Fine Particulate Matter

• Authors: Natália de Souza Xavier Costa, Universidade de São Paulo; Gabriel Ribeiro Júnior, Universidade de São Paulo; Adair Aparecida dos Santos Alemany, Universidade de São Paulo; Luciano Belotti, Universidade de São Paulo; Marcela Frota Cavalcante, Universidade de São Paulo; Susan Ribeiro, Emory University; Mariana M Veras, Universidade de São Paulo; Esper Georges Kallás, Universidade de São Paulo; Paulo Hilário Nascimento Saldiva, Universidade de São Paulo; Marisa Dolhnikoff, Universidade de São Paulo; Luiz Fernando Ferraz da Silva, Universidade de São Paulo
• Journal Title: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
• Volume: Volume 23, Number 7
• Publisher: MDPI AG | 2022-04-01
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.3390/ijms23073913
• Subjects: Health Sciences, Pathology
• Keywords: air pollution; acute lung injury; lipopolysaccharides; inflammatory response

Abstract

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-1β, 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-1β, 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.