ArticleScientific reports2018
Bushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Non-respiratory health risks and mortality associated with fighting bushfires (wildfires): a systematic review.International archives of occupational and environmental health · 2025Pooled it
- Chemical complexity and enrichment in wildland-urban interface fire emissions: A case study of particulate matter, gas-phase pollutants, and ash from the 2025 Los Angeles fires.Journal of hazardous materials · 2026Article
- Impact of Canadian Wildfire-Emitted Particulate Matter on THP-1 Lung Macrophage Health and Function.Environmental science & technology · 2025Article
- Eucalyptus Wood Smoke Extract Elicits a Dose-Dependent Effect in Brain Endothelial Cells.International journal of molecular sciences · 2024Article
- Reduction in Rubicon by cigarette smoke is associated with impaired phagocytosis and occurs through lysosomal degradation pathway.Clinical and experimental medicine · 2023Article
- Effects of wildfire smoke PM2.5 on indicators of inflammation, health, and metabolism of preweaned Holstein heifers.Journal of animal science · 2023Article
- Impact of JAK/STAT inhibitors on human monocyte-derived-macrophages stimulated by cigarette smoke extract and lipopolysaccharide.Clinical and experimental pharmacology & physiology · 2022Article
- Air pollution and cardiovascular disease: Can the Australian bushfires and global COVID-19 pandemic of 2020 convince us to change our ways?BioEssays : news and reviews in molecular, cellular and developmental biology · 2021Review
- Physical and Mental Health Effects of Bushfire and Smoke in the Australian Capital Territory 2019-20.Frontiers in public health · 2021Article
- In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure.Journal of visualized experiments : JoVE · 2019Article
- Tumor-derived nanovesicles promote lung distribution of the therapeutic nanovector through repression of Kupffer cell-mediated phagocytosis.Theranostics · 2019Article
- Regulation of Apoptotic Cell Clearance During Resolution of Inflammation.Frontiers in pharmacology · 2019Review
- Health risks of climate change in Australia: An umbrella review.The journal of climate change and healthReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.