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Departments of 1 Surgery and
2 Pathology,
Received 12 November 1996; accepted in final form 16 May 1997.
Weiser, Martin R., Taine T. V. Pechet, Julian P. Williams,
Minghe Ma, Paul S. Frenette, Francis D. Moore, Lester Kobzik, Richard
O. Hines, Denisa D. Wagner, Michael C. Carroll, and Herbert B. Hechtman. Experimental murine acid aspiration injury is mediated
by neutrophils and the alternative complement pathway. J. Appl. Physiol. 83(4):
1090-1095, 1997.
complement activation; transgenic mice; inflammation; pneumonia; selectins
Acid aspiration may result in the development of
the acute respiratory distress syndrome, an event associated with
significant morbidity and mortality. Although once attributed to direct
distal airway injury, the pulmonary failure after acid aspiration is
more complex and involves an inflammatory injury mediated by complement
(C) and polymorphonuclear leukocytes. This study examines the injurious
inflammatory cascades that are activated after acid aspiration. The
role of neutrophils was defined by immunodepletion before aspiration,
which reduced injury by 59%. The injury was not modified in either P-
or E-selectin-knockout mice, indicating that these adhesion molecules
were not operative. C activation after aspiration was documented with
immunochemistry by C3 deposition on injured alveolar pneumocytes.
Animals in which C activation was inhibited with soluble C receptor
type 1 (sCR1) had a 54% reduction in injury, similar to the level of
protection seen in C3-knockout mice (58%). However C4-knockout mice
were not protected from injury, indicating that C activation is
mediated by the alternative pathway. Finally, an additive effect of
neutrophils and C was demonstrated whereby neutropenic animals that
were treated with sCR1 showed an 85% reduction in injury. Thus acid
aspiration injury is mediated by neutrophils and the alternative C
pathway.
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society
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