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J Appl Physiol 87: 2357-2361, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 6, 2357-2361, December 1999

Membrane attack complex of complement and neutrophils mediate the injury of acid aspiration

Constantinos Kyriakides1, William Austen Jr.1, Yong Wang1, Joanne Favuzza1, Lester Kobzik2, Francis D. Moore Jr.1, and Herbert B. Hechtman1

Departments of 1 Surgery and 2 Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115

A significant role for the alternative complement pathway in acid aspiration has been demonstrated by the observation that C3 genetic knockout mice are protected from injury. Utilizing C5-deficient mice, we now test the role of the terminal complement components in mediating injury. Lung permeability in C5-deficient mice was 64% less than in wild-type animals and was similar to wild-type mice treated with soluble complement receptor type 1, which gave a 67% protection. Injury was fully restored in C5-deficient mice reconstituted with wild-type serum. The role of neutrophils was established in immunodepleted wild-type animals that showed a 58% protection. Injury was further reduced (90%) with the addition of soluble complement receptor type 1, indicating an additive effect of neutrophils and complement. Similarly, an additional protection was noted in C5-deficient neutropenic mice, indicating that neutrophil-mediated injury does not require C5a. Thus acid aspiration injury is mediated by the membrane attack complex and neutrophils. Neutrophil activity is independent of C5a.

inflammation; complement activation; polymorphonuclear leukocytes; pneumonia; murine


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