LUNG HYALURONAN DECREASES DURING GROUP-B STREPTOCOCCAL PNEUMONIA IN NEONATAL PIGLETS

Neonatal Group B streptococcus (GBS) sepsis and pneumonia result in lu ng injury and remain a major cause of morbidity and mortality in the n ewborn. Increased lung hyaluronan (HA) content is an important compone nt of the lung's early response to damage in diseases such as adult re spiratory distress syndrome (ARDS), infant respiratory distress syndro me (IRDS), and bleomycin-induced fibrosis. It is known, however, that GBS virulence factors include specific secretory enzymes such as hyalu ronidase, an enzyme which breaks down HA. We therefore hypothesized th at in lobar GBS pneumonia, lung HA would be decreased compared with no rmal values, and that in lobar pneumonia with atelectasis, lung HA wou ld be further decreased because of increased substrate availability. T he right lower lobes (RLL) and left lower lobes (LLL) of anesthetized piglets 16 +/- 2 d old were each selectively inoculated with 1 x 10(9) colony-forming units (CFU) GBS via an endobronchial catheter (n = 7). The LLL was subsequently collapsed by endobronchial occlusion followi ng 10 min of 100% O-2. Control animals (n = 6) were anesthetized, inst rumented, and ventilated without exposure to GBS. At 4 h, lungs were r emoved and HA extracted and assayed using a competitive inhibition ass ay. HA extracted from areas of lobar pneumonia was significantly decre ased (27 +/- 6.6 mu g/g wet lung, p < 0.005) when compared with contro l values of control piglets (51 +/- 19.6 mu g/g wet lung). Atelectasis plus lobar pneumonia further decreased lung HA to 10 +/- 13.3 mu g/g wet lung, p < 0.0001. We conclude that lobar GBS decreases lung HA and that this process is augmented by collapsed lung regions, and specula te that this departure from the usual early lung response to injury co ntributes to GBS invasion of lung parenchyma.