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Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function

Bushfires are increasing in frequency and severity worldwide. Bushfire smoke contains organic/inorganic compounds including aldehydes and acrolein. We described suppressive effects of tobacco smoke on the phagocytic capacity of airway macrophages, linked to secondary necrosis of uncleared apoptotic...

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Autores principales: Hamon, Rhys, Tran, Hai B., Roscioli, Eugene, Ween, Miranda, Jersmann, Hubertus, Hodge, Sandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128914/
https://www.ncbi.nlm.nih.gov/pubmed/30194323
http://dx.doi.org/10.1038/s41598-018-31459-6
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author Hamon, Rhys
Tran, Hai B.
Roscioli, Eugene
Ween, Miranda
Jersmann, Hubertus
Hodge, Sandra
author_facet Hamon, Rhys
Tran, Hai B.
Roscioli, Eugene
Ween, Miranda
Jersmann, Hubertus
Hodge, Sandra
author_sort Hamon, Rhys
collection PubMed
description Bushfires are increasing in frequency and severity worldwide. Bushfire smoke contains organic/inorganic compounds including aldehydes and acrolein. We described suppressive effects of tobacco smoke on the phagocytic capacity of airway macrophages, linked to secondary necrosis of uncleared apoptotic epithelial cells, persistence of non-typeable H. influenzae (NTHi), and inflammation. We hypothesised that bushfire smoke extract (BFSE) would similarly impair macrophage function. THP-1 or monocyte-derived macrophages (MDM) were exposed to 1–10% BFSE prepared from foliage of 5 common Australian native plants (genus Acacia or Eucalyptus), or 10% cigarette smoke extract (CSE). Phagocytic recognition receptors were measured by flow cytometry; pro-inflammatory cytokines and caspase 1 by immunofluorescence or cytometric bead array; viability by LDH assay; and capsase-3/PARP by western blot. BFSE significantly decreased phagocytosis of apoptotic cells or NTHi by both THP-1 macrophages and MDM vs air control, consistent with the effects of CSE. BFSE significantly decreased MDM expression of CD36, CD44, SR-A1, CD206 and TLR-2 and increased active IL-1β, caspase-1 and secreted IL-8. BFSE dose-dependently decreased THP-1 macrophage viability (5-fold increase in LDH at 10%) and significantly increased active caspase-3. BFSE impairs macrophage function to a similar extent as CSE, highlighting the need for further research, especially in patients with pre-existing lung disease.
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spelling pubmed-61289142018-09-10 Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function Hamon, Rhys Tran, Hai B. Roscioli, Eugene Ween, Miranda Jersmann, Hubertus Hodge, Sandra Sci Rep Article Bushfires are increasing in frequency and severity worldwide. Bushfire smoke contains organic/inorganic compounds including aldehydes and acrolein. We described suppressive effects of tobacco smoke on the phagocytic capacity of airway macrophages, linked to secondary necrosis of uncleared apoptotic epithelial cells, persistence of non-typeable H. influenzae (NTHi), and inflammation. We hypothesised that bushfire smoke extract (BFSE) would similarly impair macrophage function. THP-1 or monocyte-derived macrophages (MDM) were exposed to 1–10% BFSE prepared from foliage of 5 common Australian native plants (genus Acacia or Eucalyptus), or 10% cigarette smoke extract (CSE). Phagocytic recognition receptors were measured by flow cytometry; pro-inflammatory cytokines and caspase 1 by immunofluorescence or cytometric bead array; viability by LDH assay; and capsase-3/PARP by western blot. BFSE significantly decreased phagocytosis of apoptotic cells or NTHi by both THP-1 macrophages and MDM vs air control, consistent with the effects of CSE. BFSE significantly decreased MDM expression of CD36, CD44, SR-A1, CD206 and TLR-2 and increased active IL-1β, caspase-1 and secreted IL-8. BFSE dose-dependently decreased THP-1 macrophage viability (5-fold increase in LDH at 10%) and significantly increased active caspase-3. BFSE impairs macrophage function to a similar extent as CSE, highlighting the need for further research, especially in patients with pre-existing lung disease. Nature Publishing Group UK 2018-09-07 /pmc/articles/PMC6128914/ /pubmed/30194323 http://dx.doi.org/10.1038/s41598-018-31459-6 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Hamon, Rhys
Tran, Hai B.
Roscioli, Eugene
Ween, Miranda
Jersmann, Hubertus
Hodge, Sandra
Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
title Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
title_full Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
title_fullStr Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
title_full_unstemmed Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
title_short Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
title_sort bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128914/
https://www.ncbi.nlm.nih.gov/pubmed/30194323
http://dx.doi.org/10.1038/s41598-018-31459-6
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