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Comparison of fluticasone propionate and budesonide on COPD macrophage and neutrophil function
Kylie Br Belchamber1, Catherine Mr Thomas1, Amy E Dunne1
1Airway Disease Section, National Heart and Lung Institute, Dovehouse Street, Imperial College London, London, UK, l.donnelly@imperial.ac.uk.
Background:
Inhaled corticosteroid use is associated with increased rates of pneumonia in COPD patients. The underlying mechanism is unknown, although recent data suggest that pneumonia is more frequent in patients treated with fluticasone propionate (FP) than budesonide. Macrophages and neutrophils from COPD patients are deficient in clearing bacteria, and this might explain increased bacterial colonization in COPD. Inhaled corticosteroid may further suppress this response; therefore, we examined the effect of FP and budesonide on phagocytosis of common respiratory pathogens by monocyte-derived macrophages (MDMs) and neutrophils.
Methods:
MDMs from COPD patients (n=20-24) were preincubated with FP or budesonide for 1 or 18 hours, after which phagocytosis of fluorescently labeled inert beads or heat-killed Haemophilus influenzae/Streptococcus pneumoniae were measured fluorimetrically after 1 or 4 hours. Additionally, CXCL8, IL6, and TNFα concentrations in supernatants by ELISA, MDM-scavenger-receptor expression by flow cytometry, and MDM ability to kill bacteria were measured. Neutrophils from COPD patients (n=8) were preincubated with corticosteroids for 1 hour and bacteria phagocytosis measured by flow cytometry.
Results:
After 1 hour's preincubation, neither corticosteroid altered MDM phagocytosis of beads or H. influenzae; however, budesonide (10-7 M) increased S. pneumoniae phagocytosis by 23% (P<0.05). After 18 hours' preincubation, neither corticosteroid altered MDM phagocytosis of any prey, although H. influenzae phagocytosis by budesonide was significantly greater compared to FP at 10-6 and 10-5 M (P<0.05). The 1-hour preincubation with either corticosteroid inhibited bacteria-induced CXCL8 release (at 10-7 and 10-5 M, P<0.05); however, this effect was lost at 18-hour preincubation. There was no change in receptor expression, bacterial killing, or neutrophil phagocytosis by either corticosteroid.
Conclusion:
These data suggest that dissolved FP and budesonide do not have an overall effect on MDM or neutrophil phagocytosis of bacteria.
Insights
Inhaled corticosteroids like fluticasone propionate (FP) and budesonide do not significantly impact the ability of immune cells from COPD patients to engulf bacteria. This suggests other mechanisms may explain increased pneumonia risk in COPD patients using these drugs.
Area of Science:
- Immunology
- Pharmacology
- Respiratory Medicine
Background:
- Inhaled corticosteroid (ICS) use is linked to higher pneumonia rates in COPD patients.
- Fluticasone propionate (FP) may be associated with more pneumonia than budesonide.
- COPD patients' macrophages and neutrophils have impaired bacterial clearance, potentially worsened by ICS.
Purpose of the Study:
- To investigate the effects of FP and budesonide on phagocytosis of respiratory pathogens by macrophages and neutrophils from COPD patients.
- To determine if ICS influence bacterial clearance mechanisms in COPD.
Main Methods:
- Monocyte-derived macrophages (MDMs) and neutrophils from COPD patients were incubated with FP or budesonide.
- Phagocytosis of bacteria and beads by MDMs and neutrophils was measured.
- Cytokine release, receptor expression, and bacterial killing capacity were assessed.
Main Results:
- Short-term budesonide exposure enhanced S. pneumoniae phagocytosis by MDMs.
- Longer exposure showed budesonide had a greater effect on H. influenzae phagocytosis than FP.
- ICS transiently inhibited bacteria-induced CXCL8 release but did not affect overall phagocytosis, bacterial killing, or neutrophil phagocytosis.
Conclusions:
- Dissolved FP and budesonide do not broadly impair MDM or neutrophil phagocytosis of bacteria in COPD patients.
- The study did not find evidence that these ICS directly suppress key phagocytic functions relevant to bacterial clearance.
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