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Am J Physiol Lung Cell Mol Physiol 285: L854-L861, 2003. First published June 6, 2003; doi:10.1152/ajplung.00439.2002
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Surfactant protein A enhances apoptotic cell uptake and TGF-{beta}1 release by inflammatory alveolar macrophages

Michael F. Reidy1 and Jo Rae Wright2

1Division of Pulmonary and Critical Care Medicine and 2Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710

Submitted 18 December 2002 ; accepted in final form 3 June 2003

The phagocytosis of apoptotic inflammatory cells by alveolar macrophages (AMs) is a key component of inflammation resolution within the air space. Surfactant protein A (SP-A) has been shown to stimulate the phagocytosis of apoptotic neutrophils (PMNs) by normal AMs. We hypothesized that SP-A promotes the resolution of alveolar inflammation by enhancing apoptotic PMN phagocytosis and anti-inflammatory cytokine release by inflammatory AMs. Using an LPS lung inflammation model, we determined that SP-A stimulates the phagocytosis of apoptotic PMNs threefold by normal AMs and AMs isolated after LPS injury. Furthermore, SP-A enhances transforming growth factor-{beta}1 (TGF-{beta}1) release from both AM populations. Inflammatory AMs release twofold more TGF-{beta}1 in culture than do normal AMs. SP-A and apoptotic PMNs together stimulate TGF-{beta}1 release equivalently from normal and inflammatory cultured AMs (330% of unstimulated release by normal AMs). In summary, SP-A enhances apoptotic PMN uptake, stimulates AM TGF-{beta}1 release, and modulates the amount of TGF-{beta}1 released when AMs phagocytose apoptotic PMNs. These findings support the hypothesis that SP-A promotes the resolution of alveolar inflammation.

lipopolysaccharide; innate immunity; collectin; apoptosis; transforming growth factor-{beta}1


Address for reprint requests and other correspondence: J. R. Wright, Box 3709, Duke University Medical Center, Durham, NC 27710 (E-mail: j.wright{at}cellbio.duke.edu).




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