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Cardiovascular Research Institute, University of California, San Francisco, California 94143-0130
Received 11 July 1996; accepted in final form 3 February 1997.
Folkesson, Hans G., and Michael A. Matthay. Inhibition
of CD18 or CD11b attenuates acute lung injury after acid instillation in rabbits. J. Appl. Physiol. 82(6):
1743-1750, 1997.
Acid-induced lung injury is mediated
primarily by activated neutrophils. Although a prior study demonstrated
that acid-induced neutrophil influx into the air spaces was not CD18
dependent, we hypothesized that either a neutralizing anti-CD18
monoclonal antibody (MHM23) or a neutrophil inhibitory factor (NIF),
NIF (CD11b,18), might attenuate acid-induced lung injury in rabbits by
interfering with neutrophil activation. This hypothesis derived from in
vitro studies that reported that anti-CD18 therapy prevented tumor
necrosis factor-
-induced neutrophil activation. Hydrochloric acid
(pH = 1.5 in one-third normal saline) or one-third normal saline (4 ml/kg) was instilled into the lungs of ventilated, anesthetized
rabbits. The rabbits were studied for 6 h. In acid-instilled rabbits
without the anti-CD18 monoclonal antibody or NIF (CD11b,18), severe
lung injury developed. In acid-instilled rabbits, pretreatment (5 min
before acid) with the anti-CD18 monoclonal antibody (2 mg/kg iv) or
pretreatment with the NIF (anti-CD11b,18, 10 mg/kg iv) prevented
50-70% of acid-induced abnormalities in oxygenation, the increase
in extravascular lung water, and extravascular protein accumulation.
The anti-CD18 monoclonal antibody was associated with a significant
increase in air space neutrophils by bronchoalveolar lavage, suggesting that the neutrophils respond normally to chemotactic stimuli but that
the neutrophils did not injure the lung even though they accumulated in
the air spaces. In summary, neutralization of CD18 attenuates the acute
lung injury after acid instillation without reducing the number of
neutrophils in the air spaces, suggesting that anti-CD18 therapy may be
beneficial because of its capacity to reduce neutrophil activation.
pulmonary edema; hydrochloric acid; lung endothelial permeability; neutrophil inhibitory factor
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