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Thus, efferocytosis requires the AM to adopt an anti-inflammatory state in order to prevent inflammatory responses to self-proteins.92 Efferocytosis is reduced in AMs from smokers compared with never-smokers.93 AMs recognise apoptotic cells using cell surface receptors including CD44 (hyaluronan receptor), which is expressed at lower levels in smokers38 and is important for clearance of apoptotic neutrophils and the release of anti-inflammatory and pro-repair mediators such as TGF-.94 CS has been shown to reduce efferocytosis in AMs through the interaction of AM with CS modified ECM proteins and aberrant surfactant processing.95 Defective efferocytosis of AMs may also be driven by the significantly increased levels of CS-induced oxidative stress.96 Another mechanism for reduced efferocytosis may be due to CS-induced defects in phagosome and the lysosome fusion, demonstrated in rat models.97 CS-reduced AM efferocytosis was restored through the delivery of GM-CSF to the alveolar space and was associated with reduced morbidity following influenza infection.98 In patients with COPD, AM efferocytosis was higher than in those who stopped smoking compared with those who continued to smoke, suggesting a CS-related effect on AM in COPD that may be partially resolved on smoking cessation.38 Following community acquired pneumonia, smokers had reduced AM efferocytosis, as were those who were not on a statin

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