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Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro
Epidemiological evidence has shown the association between exposure to ambient fine particulate matter (PM) and increased susceptibility to bacterial and viral respiratory infections. However, to date, the underlying mechanisms of immunomodulatory effects of PM remain unclear. Our objective was to e...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7516585/ https://www.ncbi.nlm.nih.gov/pubmed/32980306 http://dx.doi.org/10.1016/j.envres.2020.110244 |
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author | Shahbaz, Muhammad Ali Martikainen, Maria-Viola Rönkkö, Teemu J. Komppula, Mika Jalava, Pasi I. Roponen, Marjut |
author_facet | Shahbaz, Muhammad Ali Martikainen, Maria-Viola Rönkkö, Teemu J. Komppula, Mika Jalava, Pasi I. Roponen, Marjut |
author_sort | Shahbaz, Muhammad Ali |
collection | PubMed |
description | Epidemiological evidence has shown the association between exposure to ambient fine particulate matter (PM) and increased susceptibility to bacterial and viral respiratory infections. However, to date, the underlying mechanisms of immunomodulatory effects of PM remain unclear. Our objective was to explore how exposure to relatively low doses of urban air PM alters innate responses to bacterial and viral stimuli in vitro. We used secondary alveolar epithelial cell line along with monocyte-derived macrophages to replicate innate lung barrier in vitro. Co-cultured cells were first exposed for 24 h to PM(2.5-1) (particle aerodynamic diameter between 1 and 2.5 μm) and subsequently for an additional 24 h to lipopolysaccharide (TLR4), polyinosinic-polycytidylic acid (TLR3), and synthetic single-stranded RNA oligoribonucleotides (TLR7/8) to mimic bacterial or viral stimulation. Toxicological endpoints included pro-inflammatory cytokines (IL-8, IL-6, and TNF-α), cellular metabolic activity, and cell cycle phase distribution. We show that cells exposed to PM(2.5-1) produced higher levels of pro-inflammatory cytokines following stimulation with bacterial TLR4 ligand than cells exposed to PM(2.5-1) or bacterial ligand alone. On the contrary, PM(2.5-1) exposure reduced pro-inflammatory responses to viral ligands TLR3 and TLR7/8. Cell cycle analysis indicated that viral ligands induced cell cycle arrest at the G2-M phase. In PM-primed co-cultures, however, they failed to induce the G2-M phase arrest. Contrarily, bacterial stimulation caused a slight increase in cells in the sub-G1 phase but in PM(2.5-1) primed co-cultures the effect of bacterial stimulation was masked by PM(2.5-1.) These findings indicate that PM(2.5-1) may alter responses of immune defense differently against bacterial and viral infections. Further studies are required to explain the mechanism of immune modulation caused by PM in altering the susceptibility to respiratory infections. |
format | Online Article Text |
id | pubmed-7516585 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Elsevier Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-75165852020-09-25 Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro Shahbaz, Muhammad Ali Martikainen, Maria-Viola Rönkkö, Teemu J. Komppula, Mika Jalava, Pasi I. Roponen, Marjut Environ Res Article Epidemiological evidence has shown the association between exposure to ambient fine particulate matter (PM) and increased susceptibility to bacterial and viral respiratory infections. However, to date, the underlying mechanisms of immunomodulatory effects of PM remain unclear. Our objective was to explore how exposure to relatively low doses of urban air PM alters innate responses to bacterial and viral stimuli in vitro. We used secondary alveolar epithelial cell line along with monocyte-derived macrophages to replicate innate lung barrier in vitro. Co-cultured cells were first exposed for 24 h to PM(2.5-1) (particle aerodynamic diameter between 1 and 2.5 μm) and subsequently for an additional 24 h to lipopolysaccharide (TLR4), polyinosinic-polycytidylic acid (TLR3), and synthetic single-stranded RNA oligoribonucleotides (TLR7/8) to mimic bacterial or viral stimulation. Toxicological endpoints included pro-inflammatory cytokines (IL-8, IL-6, and TNF-α), cellular metabolic activity, and cell cycle phase distribution. We show that cells exposed to PM(2.5-1) produced higher levels of pro-inflammatory cytokines following stimulation with bacterial TLR4 ligand than cells exposed to PM(2.5-1) or bacterial ligand alone. On the contrary, PM(2.5-1) exposure reduced pro-inflammatory responses to viral ligands TLR3 and TLR7/8. Cell cycle analysis indicated that viral ligands induced cell cycle arrest at the G2-M phase. In PM-primed co-cultures, however, they failed to induce the G2-M phase arrest. Contrarily, bacterial stimulation caused a slight increase in cells in the sub-G1 phase but in PM(2.5-1) primed co-cultures the effect of bacterial stimulation was masked by PM(2.5-1.) These findings indicate that PM(2.5-1) may alter responses of immune defense differently against bacterial and viral infections. Further studies are required to explain the mechanism of immune modulation caused by PM in altering the susceptibility to respiratory infections. Elsevier Inc. 2021-01 2020-09-25 /pmc/articles/PMC7516585/ /pubmed/32980306 http://dx.doi.org/10.1016/j.envres.2020.110244 Text en © 2020 Elsevier Inc. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Shahbaz, Muhammad Ali Martikainen, Maria-Viola Rönkkö, Teemu J. Komppula, Mika Jalava, Pasi I. Roponen, Marjut Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro |
title | Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro |
title_full | Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro |
title_fullStr | Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro |
title_full_unstemmed | Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro |
title_short | Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro |
title_sort | urban air pm modifies differently immune defense responses against bacterial and viral infections in vitro |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7516585/ https://www.ncbi.nlm.nih.gov/pubmed/32980306 http://dx.doi.org/10.1016/j.envres.2020.110244 |
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