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Publication : Extracellular superoxide dismutase in macrophages augments bacterial killing by promoting phagocytosis.

First Author  Manni ML Year  2011
Journal  Am J Pathol Volume  178
Issue  6 Pages  2752-9
PubMed ID  21641397 Mgi Jnum  J:173474
Mgi Id  MGI:5014128 Doi  10.1016/j.ajpath.2011.02.007
Citation  Manni ML, et al. (2011) Extracellular superoxide dismutase in macrophages augments bacterial killing by promoting phagocytosis. Am J Pathol 178(6):2752-9
abstractText  Extracellular superoxide dismutase (EC-SOD) is abundant in the lung and limits inflammation and injury in response to many pulmonary insults. To test the hypothesis that EC-SOD has an important role in bacterial infections, wild-type and EC-SOD knockout (KO) mice were infected with Escherichia coli to induce pneumonia. Although mice in the EC-SOD KO group demonstrated greater pulmonary inflammation than did wild-type mice, there was less clearance of bacteria from their lungs after infection. Macrophages and neutrophils express EC-SOD; however, its function and subcellular localization in these inflammatory cells is unclear. In the present study, immunogold electron microscopy revealed EC-SOD in membrane-bound vesicles of phagocytes. These findings suggest that inflammatory cell EC-SOD may have a role in antibacterial defense. To test this hypothesis, phagocytes from wild-type and EC-SOD KO mice were evaluated. Although macrophages lacking EC-SOD produced more reactive oxygen species than did cells expressing EC-SOD after stimulation, they demonstrated significantly impaired phagocytosis and killing of bacteria. Overall, this suggests that EC-SOD facilitates clearance of bacteria and limits inflammation in response to infection by promoting bacterial phagocytosis.
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