ABSTRACT. Despite the serious pulmonary manifestaintact animal could be initiated by a direct interaction tions of early onset group B streptococcal (GBS) sepsis, it between GBS and resident lung cells without obligatory is not known whether the organism distributes into lung participation by other organ systems. (Pediatr Res 27: tissue and whether adverse pulmonary hemodynamic ab-344-348,1990) normalities relate to an interaction between the organism and target cells in the pulmonary vascular bed. AccordAbbreviations ingly, this study evaluated the distribution and fate of GBS in the lung, liver, and spleen of anesthetized infant piglets GBS, group B streptococcus and in isolated, salt solution-perfused piglet lung prepara-HBSS, Hanks' balanced salt solution tions. GBS were radiolabeled with lllIndium-oxine and cfu, colony-forming unit infused at a dose of 108 organisms/kg/min for 15 min into Ppa, pulmonary arterial pressure anesthetized piglets ranging in age from 5-10 d. Forty-five Pla, left atrial pressure min after termination of the infusion, animals were killed Rt, total resistance and specimens of lung, liver, spleen, and blood were excised Ra, arterial resistance and the relative deposition and viability of GBS were Rv, venous resistance determined. Most of the recovered bacteria were detected Pdo, double occlusion pressure in the lung (53.2 f 3.9%) followed by the liver (41.4 f 2.0%) and spleen (2.2 f 0.38%). GBS detected in the blood was estimated to be only 3.2 2 1.0% of the infused dose. Viability of GBS was least in the lung (21.4 2 2.6%)The question is straight-forward: Does GBS promote pulmorelative to the liver (45.7 f 11.2%) and spleen (83.4 +: nary hypertension in the newborn through interaction with a 19.5%). After a 60-min GBS infusion, transmission elec-target cell in the lung? The concept that GBS-induced pulmonary tron microscopy localized the organism within pulmonary hypertension results from an interaction with resident lung cells intravascular macrophages in the lung; there was no evi-is intuitively appealing. The lung contains several cell types that dence for bacterial interaction with either neutrophils or could serve as transducers of the pulmonary hemodynamic reendothelial cells. In the liver, GBS was found exclusively sponse to GBS. For example, the lung contains a substantial in Kupffer cells. In isolated piglet lungs perfused at a population of marginated neutrophils, a phagocytic cell known constant flow rate with blood-free physiologic salt solution, to elaborate various mediators incriminated in the response to GBS (lo6 to 10' organisms/mL) provoked concentration-GBS (I), including thromboxane AZ, sulfidopeptide leukotrienes, dependent increases in pulmonary vascular resistance. and toxic oxygen radicals (2-4). Pulmonary vascular endothelial Transmission electron microscopic examination of isolated cells also exhibit phagocytic activity ( 5 , 6) and produce eicosalungs indicated that GBS was localized within pulmonary noids with chemoattractant activity for neutrophils (7)....