Pathophysiology of neonatal lung injury induced by monoclonal antibody to surfactant protein B

Near-term newborn rabbits were exposed via the airways to a monoclonal antibody to surfactant protein B and ventilated for 0-120 min. Control animals received nonspecific rabbit or mouse immunoglobulin G, saline, or no material via the airways. Administration of the antibody at greater than or equal to 40 mg/kg elicited an immediate, significant fall in lung-thorax compliance associated with progressive intra-alveolar edema and/or alveolar collapse and necrosis and desquamation of airway epithelium, and hyaline membranes. The vascular-to-alveolar leak of human albumin and human immunoglobulin G, injected intravenously at birth and determined in lung lavage fluid 60-120 min after instillation of the antibody, was 1.8% for the left lung, with no difference between the markers. The average leak in control animals ventilated for 120 min was <0.3% (P < 0.05). Cytospin preparations of lung lavage fluid from animals exposed to the antibody showed significantly increased recruitment of neutrophilic granulocytes. The pathology and pathophysiology of neonatal lung injury induced by the monoclonal antibody to surfactant protein B probably reflect a combination of direct inactivation of surfactant and an inflammatory response triggered by the immune reaction.