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Macrophage Elastase Prevents Gemella morbillorum Infection and Improves Outcome Following Murine Bone Marrow Transplantation*

W. Hartzell, MD; S. D. Shapiro, MD
Author and Funding Information

*From the Departments of Medicine and Cell Biology, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, MO.

Correspondence to: William Hartzell, MD, Pulmonary and Critical Care, Washington University, 216 S Kingshighway Blvd, St. Louis, MO 63110



Chest. 1999;116(suppl_1):31S-32S. doi:10.1378/chest.116.suppl_1.31S-a
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Lung injury after bone marrow transplant (BMT) is a major cause of morbidity and mortality limiting the benefits of this procedure. One type of lung injury, idiopathic pneumonia syndrome, has been found to contain abundant expression of a macrophage-derived metalloproteinase, macrophage elastase (ME), in human lung biopsy specimens. To determine the role of ME in post-BMT lung injury, we developed a murine BMT model using wild-type (MME+/+) and mice deficient in ME (MME−/−), generated by gene targeting. Allogeneic single major histocompatibility complex mismatched BMTs were performed to replicate conditions that lead to lung injury.


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