| First Author | LeVine AM | Year | 1999 |
| Journal | J Clin Invest | Volume | 103 |
| Issue | 4 | Pages | 563-9 |
| PubMed ID | 10021465 | Mgi Jnum | J:119613 |
| Mgi Id | MGI:3702842 | Doi | 10.1172/JCI5212 |
| Citation | LeVine AM, et al. (1999) GM-CSF-deficient mice are susceptible to pulmonary group B streptococcal infection. J Clin Invest 103(4):563-9 |
| abstractText | Granulocyte-macrophage colony-stimulating factor (GM-CSF) gene-targeted mice (GM-/-) cleared group B streptococcus (GBS) from the lungs more slowly than wild-type mice. Expression of GM-CSF in the respiratory epithelium of GM-/- mice improved bacterial clearance to levels greater than that in wild-type GM+/+ mice. Acute aerosolization of GM-CSF to GM+/+ mice significantly enhanced clearance of GBS at 24 hours. GBS infection was associated with increased neutrophilic infiltration in lungs of GM-/- mice, while macrophage infiltrates predominated in wild-type mice, suggesting an abnormality in macrophage clearance of bacteria in the absence of GM-CSF. While phagocytosis of GBS was unaltered, production of superoxide radicals and hydrogen peroxide was markedly deficient in macrophages from GM-/- mice. Lipid peroxidation, assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice. GM-CSF plays an important role in GBS clearance in vivo, mediated in part by its role in enhancing superoxide and hydrogen peroxide production and bacterial killing by alveolar macrophages. |
