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.
Highlights
Bushfire severity and frequency is increasing worldwide and further increases are predicted
We found that cigarette smoke exposure inhibited the capacity of alveolar macrophages to phagocytose bacteria, including non-typeable H. influenzae (NTHi), a common coloniser of the airway in chronic lung diseases that is associated with significant morbidity
We hypothesised that exposure to a bushfire smoke extract (BFSE) causes defects in macrophage function that parallel our findings with cigarette smoke extract (CSE)
Summary
Bushfire severity and frequency is increasing worldwide and further increases are predicted. An Australian based study conducted by Martin et al.[9,10] reported increased hospital admissions for pre-existing respiratory morbidities in association with bushfire events; 13% for chronic obstructive pulmonary disease (COPD) and 12% for asthma. Similar defects were noted in patients with chronic lung diseases including COPD, severe asthma, and childhood non-CF bronchiectasis[22,23,24] This defect was associated with secondary necrosis of the uncleared material, potentially leading to release of toxic cell contents, perpetuating inflammation and further tissue damage[19,25]. We found that cigarette smoke exposure inhibited the capacity of alveolar macrophages to phagocytose bacteria, including non-typeable H. influenzae (NTHi), a common coloniser of the airway in chronic lung diseases that is associated with significant morbidity. We hypothesised that exposure to a bushfire smoke extract (BFSE) causes defects in macrophage function that parallel our findings with cigarette smoke extract (CSE)
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