The Role of Granulocytes in the Pulmonary Response to Group B Streptococcal Toxin in Young Lambs
- 1 February 1987
- journal article
- research article
- Published by Springer Nature in Pediatric Research
- Vol. 21 (2) , 159-165
- https://doi.org/10.1203/00006450-198702000-00010
Abstract
Marked leukopenia and sequestration of granulocytes in the lung are consistently seen in serve early onset group B streptococcal (GBS) disease in human infants. To investigate the role of granulocytes as potential mediators in the pulmonary pathophysiology of this disease, the effects of intracenously adminstered GBS type III toxin were studied in young lambs before and after granulocyte depletion with hydroxyurea. Granulocyte depletion markedly reduced the 4-fold increase in total lung resistance and the decrease in dynamic compliance observed after GBS toxin. Granulocyte depletion significantluy attenuated the pulmonary hypertension, hypoxema and increased minute ventilation present during the first phase of the response (0.5-1 h after GBS toxin). It did not significantly alter the increase in lung lymph flow and protein clearance during the second phase of the response (3.5-5 h after GBS toxin). The result indicates that granulocytes are involved as, mediators of the changes in lung mechanics seen after GBS toxin infusion in young lambs. Granulocytes contribute to the pulmonary hypertension and decrease in arterial oxygenation, but other mediators appear to be responsible for the injury of the vascular endothelium.Keywords
This publication has 21 references indexed in Scilit:
- Studies on Group B β-Hemolytic Streptococcus. II. Effects on Pulmonary Hemodynamics and Vascular Permeability in Unanesthetized SheepPediatric Research, 1981
- Studies on Group B β-Hemolytic Streptococcus. I. Isolation and Partial Characterization of an Extracellular ToxinPediatric Research, 1981
- Leukocytes are required for increased lung microvascular permeability after microembolization in sheep.Circulation Research, 1981
- Complement Activation during Cardiopulmonary BypassNew England Journal of Medicine, 1981
- Thromboxane A2 Mediates Augmented Polymorphonuclear Leukocyte AdhesivenessJournal of Clinical Investigation, 1980
- LUNG INFLAMMATION INDUCED BY COMPLEMENT-DERIVED CHEMOTACTIC FRAGMENTS IN THE ALVEOLUS1980
- PULMONARY MORPHOLOGY IN A MULTI-HOSPITAL COLLABORATIVE EXTRACORPOREAL MEMBRANE-OXYGENATION PROJECT .1. LIGHT-MICROSCOPY1979
- Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.Journal of Clinical Investigation, 1978
- PROSTAGLANDINS AND LUNGPublished by Elsevier ,1978
- Hemodialysis leukopenia. Pulmonary vascular leukostasis resulting from complement activation by dialyzer cellophane membranes.Journal of Clinical Investigation, 1977