LPS Response Is Impaired by Urban Fine Particulate Matter.
Natália de Souza Xavier CostaGabriel Ribeiro JúniorAdair Aparecida Dos Santos AlemanyLuciano BelottiMarcela Frota CavalcanteSusan RibeiroMariana Matera VerasEsper Georges KallásPaulo Hilário Nascimento SaldivaMarisa DolhnikoffLuiz Fernando Ferraz da SilvaPublished in: International journal of molecular sciences (2022)
Fine particulate matter (PM 2.5 ) 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 PM 2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM 2.5 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 PM 2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM 2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM 2.5 exposure.
Keyphrases
- particulate matter
- air pollution
- inflammatory response
- lps induced
- lipopolysaccharide induced
- anti inflammatory
- cardiovascular disease
- rheumatoid arthritis
- oxidative stress
- toll like receptor
- magnetic resonance
- risk assessment
- magnetic resonance imaging
- endothelial cells
- water soluble
- risk factors
- cell death
- polycyclic aromatic hydrocarbons
- endoplasmic reticulum stress
- cell cycle arrest