Abstract
Intrapulmonary clearance of group B streptococci (GBS) occurred in term rabbits 4 and 8 h after infection; GBS growth was evident in preterm rabbits at 8 h. Bronchoalveolar lavage revealed 17-fold higher numbers of pulmonary alveolar macrophages (PAM) in term versus preterm animals immediately after infection, whereas polymorphonuclear leukocyte (PMNL) recruitment was 13-fold greater in preterm than term rabbits at 8 h. Anti-CD18 monoclonal antibody R15.7 did not reduce PMNL influx or GBS killing in term animals. R15.7 failed to inhibit PMNL influx but augmented GBS growth in preterm animals. R15.7 significantly impaired GBS phagocytosis by preterm and term PMNL in vitro but had no effect on ingestion of GBS by preterm and term PAM. Thus, GBS infection initiates PMNL recruitment into lungs of preterm rabbits by CD18-independent mechanisms, but phagocytosis of GBS by PMNL is largely CD18-dependent. The poorer outcome of GBS pneumonia in preterm versus term newborns may result from low levels of PAM, thereby mandating recruitment of PMNL as a second phagocytic defense.
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