Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 10, Pages 6947-6953Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.10.6947
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Funding
- NHLBI NIH HHS [R01 HL051856, R01 HL051854-16, HL 51854, K08 HL082742, K08 HL 82742, R01 HL051854, R37 HL051856, R37 HL051856-14, HL 51856] Funding Source: Medline
- NIAID NIH HHS [P01 AI053194, P01 AI 53194] Funding Source: Medline
- NIGMS NIH HHS [R01 GM 38330, R01 GM038330] Funding Source: Medline
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CD47 modulates neutrophil transmigration toward the sites of infection or injury. Mice lacking CD47 are susceptible to Escherichia coli (E. coli) peritonitis. However, less is known concerning the role of CD47 in the development of acute lung inflammation and injury. In this study, we show that mice lacking CD47 are protected from LPS-induced acute lung injury and E. coli pneumonia with a significant reduction in pulmonary edema, lung vascular permeability, and bacteremia. Reconstitution of CD47(+/-) mice with CD47(-/-) neutrophils significantly reduced lung edema and neutrophil infiltration, thus demonstrating that CD47(+) neutrophils are required for the development of lung injury from E. coli pneumonia. Importantly, CD47-deficient mice with E. coli pneumonia had an improved survival rate. Taken together, deficiency of CD47 protects mice from LPS-induced acute lung injury and E. coli pneumonia. Targeting CD47 may be a novel pathway for treatment of acute lung injury.
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