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2013 ; 143
(6
): 1750-1757
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Efferocytosis and lung disease
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McCubbrey AL
; Curtis JL
Chest
2013[Jun]; 143
(6
): 1750-1757
PMID23732585
show ga
In healthy individuals, billions of cells die by apoptosis each day. Clearance of
these apoptotic cells, termed "efferocytosis," must be efficient to prevent
secondary necrosis and the release of proinflammatory cell contents that disrupt
tissue homeostasis and potentially foster autoimmunity. During inflammation, most
apoptotic cells are cleared by macrophages; the efferocytic process actively
induces a macrophage phenotype that favors tissue repair and suppression of
inflammation. Several chronic lung diseases, particularly airways diseases such
as chronic obstructive lung disease, asthma, and cystic fibrosis, are
characterized by an increased lung burden of uningested apoptotic cells. Alveolar
macrophages from individuals with these chronic airways diseases have decreased
efferocytosis relative to alveolar macrophages from healthy subjects. These two
findings have led to the hypothesis that impaired apoptotic cell clearance may
contribute causally to sustained lung inflammation and that therapies to enhance
efferocytosis might be beneficial. This review of the English-language scientific
literature (2006 to mid-2012) explains how such existing therapies as
corticosteroids, statins, and macrolides may act in part by augmenting apoptotic
cell clearance. However, efferocytosis can also impede host defenses against lung
infection. Thus, determining whether novel therapies to augment efferocytosis
should be developed and in whom they should be used lies at the heart of efforts
to differentiate specific phenotypes within complex chronic lung diseases to
provide appropriately personalized therapies.
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