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1 release by inflammatory alveolar macrophages
1 Division of Pulmonary and Critical Care Medicine, Duke University Medical Center, Durham, NC, USA
2 Department of Cell Biology, Duke University Medical Center, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: j.wright{at}cellbio.duke.edu.
The phagocytosis of apoptotic inflammatory cells by alveolar macrophages (AM) is a key component of inflammation resolution within the airspace. Surfactant Protein-A (SP-A) has been shown to stimulate the phagocytosis of apoptotic neutrophils (PMN) 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 a LPS lung inflammation model, we determined that SP-A stimulates the phagocytosis of apoptotic PMNs 3-fold by normal AMs and by AMs isolated after LPS injury. Further, SP-A enhances TGF-
1 release from both AM populations. Inflammatory AMs release 2-fold more TGF-1 in culture than do normal AMs. SP-A and apoptotic PMNs together stimulate TGF-1 release equivalently from both normal and inflammatory cultured AM (330% of unstimulated release by normal AMs). In summary, SP-A enhances apoptotic PMN uptake, stimulates AM TGF-1 release, as well as modulates the amount of TGF-1 released when AMs phagocytose apoptotic PMNs. These findings support the hypothesis that SP-A promotes the resolution of alveolar inflammation.
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